Circuits that contain the Model Type : Realistic Network

(Realistic network models are those which are comparable to electrophysiology recordings, connectionist models typically describe the interaction of brain regions.)
Re-display model names without descriptions
    Models   Description
1. 2D model of olfactory bulb gamma oscillations (Li and Cleland 2017)
This is a biophysical model of the olfactory bulb (OB) that contains three types of neurons: mitral cells, granule cells and periglomerular cells. The model is used to study the cellular and synaptic mechanisms of OB gamma oscillations. We concluded that OB gamma oscillations can be best modeled by the coupled oscillator architecture termed pyramidal resonance inhibition network gamma (PRING).
2. 3D model of the olfactory bulb (Migliore et al. 2014)
This entry contains a link to a full HD version of movie 1 and the NEURON code of the paper: "Distributed organization of a brain microcircuit analysed by three-dimensional modeling: the olfactory bulb" by M Migliore, F Cavarretta, ML Hines, and GM Shepherd.
3. 3D olfactory bulb: operators (Migliore et al, 2015)
"... Using a 3D model of mitral and granule cell interactions supported by experimental findings, combined with a matrix-based representation of glomerular operations, we identify the mechanisms for forming one or more glomerular units in response to a given odor, how and to what extent the glomerular units interfere or interact with each other during learning, their computational role within the olfactory bulb microcircuit, and how their actions can be formalized into a theoretical framework in which the olfactory bulb can be considered to contain "odor operators" unique to each individual. ..."
4. 5-neuron-model of neocortex for producing realistic extracellular AP shapes (Van Dijck et al. 2012)
This is a 5-neuron model of neocortex, containing one tufted layer-5 pyramidal cell, two non-tufted pyramidal cells, and two inhibitory interneurons. It was used to reproduce extracellular spike shapes in a study comparing algorithms for spike sorting and electrode selection. The neuron models are adapted from Dyhrfjeld-Johnsen et al. (2005).
5. A 1000 cell network model for Lateral Amygdala (Kim et al. 2013)
1000 Cell Lateral Amygdala model for investigation of plasticity and memory storage during Pavlovian Conditioning.
6. A cerebellar model of phase-locked tACS for essential tremor (Schreglmann et al., 2021)
This model is a supplementary material for Schreglmann, Sebastian R., et al. "Non-invasive suppression of essential tremor via phase-locked disruption of its temporal coherence" Nature Communications (2021). The model demonstrates that phase-locked transcranial alternating current stimulation (tACS) is able to disrupt the tremor-related oscillations in the cerebellum, and its efficacy is highly dependent on the relative phase between the stimulation and tremor.
7. A computational model of action selection in the basal ganglia (Suryanarayana et al 2019)
" ... Here, we incorporate newly revealed subgroups of neurons within the GPe into an existing computational model of the basal ganglia, and investigate their role in action selection. Three main results ensued. First, using previously used metrics for selection, the new extended connectivity improved the action selection performance of the model. Second, low frequency theta oscillations were observed in the subpopulation of the GPe (the TA or ‘arkypallidal’ neurons) which project exclusively to the striatum. These oscillations were suppressed by increased dopamine activity — revealing a possible link with symptoms of Parkinson’s disease. Third, a new phenomenon was observed in which the usual monotonic relationship between input to the basal ganglia and its output within an action ‘channel’ was, under some circumstances, reversed. ..."
8. A computational model of oxytocin modulation of olfactory recognition memory (Linster & Kelsch 2019)
Model of olfactory bulb (OB) and anterior olfactory nucleus (AON) pyramidal cells. Includes olfactory sensory neurons, mitral cells, periglomerular, external tufted and granule interneurons and pyramidal cells. Can be built to include a feedback loop between OB and AON. Output consists of voltage and spikes over time in all neurons. Model can be stimulated with simulated odorants. The code submitted here has served for a number of modeling explorations of olfactory bulb and cortex. The model architecture is defined in "bulb.dat" with synapses defined in "channels.dat". The main function to run the model can be found in "neuron.c". Model architecture is constructed in "set.c" from types defined in "sim.c". A make file to create an executable is located in "neuron.mak".
9. A computational model of single-neuron perturbations (Sadeh and Clopath 2020)
A computational model to study the effect of single-neuron perturbations in large-scale excitatory-inhibitory networks of the primary visual cortex. Neuronal receptive fields and connectivity are constrained by experimental literature. The model addresses how the influence of perturbing an excitatory neuron ("influencer") in the network on other neurons ("influencees") depends on the similarity of their receptive fields. Specifically, in which regimes this influence is dominated by amplification or suppression, and how it relates to functional properties of neurons.
10. A contracting model of the basal ganglia (Girard et al. 2008)
Basal ganglia model : selection processes between channels, dynamics controlled by contraction analysis, rate-coding model of neurons based on locally projected dynamical systems (lPDS).
11. A cortico-cerebello-thalamo-cortical loop model under essential tremor (Zhang & Santaniello 2019)
We investigated the origins of oscillations under essential tremor (ET) by building a computational model of the cortico-cerebello-thalamo-cortical loop. It showed that an alteration of amplitudes and decay times of the GABAergic currents to the dentate nucleus can facilitate sustained oscillatory activity at tremor frequency throughout the network as well as a robust bursting activity in the thalamus, which is consistent with observations of thalamic tremor cells in ET patients. Tremor-related oscillations initiated in small neural populations and spread to a larger network as the synaptic dysfunction increased, while thalamic high-frequency stimulation suppressed tremor-related activity in thalamus but increased the oscillation frequency in the olivocerebellar loop.
12. A detailed and fast model of extracellular recordings (Camunas-Mesa & Qurioga 2013)
"We present a novel method to generate realistic simulations of extracellular recordings. The simulations were obtained by superimposing the activity of neurons placed randomly in a cube of brain tissue. Detailed models of individual neurons were used to reproduce the extracellular action potentials of close-by neurons. ..."
13. A detailed data-driven network model of prefrontal cortex (Hass et al 2016)
Data-based PFC-like circuit with layer 2/3 and 5, synaptic clustering, four types of interneurons and cell-type specific short-term synaptic plasticity; neuron parameters fitted to in vitro data, all other parameters constrained by experimental literature. Reproduces key features of in vivo resting state activity without specific tuning.
14. A full-scale cortical microcircuit spiking network model (Shimoura et al 2018)
Reimplementation in BRIAN 2 simulator of a full-scale cortical microcircuit containing two cell types (excitatory and inhibitory) distributed in four layers, and represents the cortical network below a surface of 1 mm² (Potjans & Diesmann, 2014).
15. A gap junction network of Amacrine Cells controls Nitric Oxide release (Jacoby et al 2018)
"... The effects of the neuromodulator nitric oxide (NO) have been studied in many circuits, including in the vertebrate retina, where it regulates synaptic release, gap junction coupling, and blood vessel dilation, but little is known about the cells that release NO. We show that a single type of amacrine cell (AC) controls NO release in the inner retina, and we report its light responses, electrical properties, and calcium dynamics. We discover that this AC forms a dense gap junction network and that the strength of electrical coupling in the network is regulated by light through NO. A model of the network offers insights into the biophysical specializations leading to auto-regulation of NO release within the network."
16. A large-scale model of the functioning brain (spaun) (Eliasmith et al. 2012)
" ... In this work, we present a 2.5-million-neuron model of the brain (called “Spaun”) that bridges this gap (between neural activity and biological function) by exhibiting many different behaviors. The model is presented only with visual image sequences, and it draws all of its responses with a physically modeled arm. Although simplified, the model captures many aspects of neuroanatomy, neurophysiology, and psychological behavior, which we demonstrate via eight diverse tasks."
17. A microcircuit model of the frontal eye fields (Heinzle et al. 2007)
" ... we show that the canonical circuit (Douglas et al. 1989, Douglas and Martin 1991) can, with a few modifications, model the primate FEF. The spike-based network of integrate-and-fire neurons was tested in tasks that were used in electrophysiological experiments in behaving macaque monkeys. The dynamics of the model matched those of neurons observed in the FEF, and the behavioral results matched those observed in psychophysical experiments. The close relationship between the model and the cortical architecture allows a detailed comparison of the simulation results with physiological data and predicts details of the anatomical circuit of the FEF."
18. A Model Circuit of Thalamocortical Convergence (Behuret et al. 2013)
“… Using dynamic-clamp techniques in thalamic slices in vitro, we combined theoretical and experimental approaches to implement a realistic hybrid retino-thalamo-cortical pathway mixing biological cells and simulated circuits. … The study of the impact of the simulated cortical input on the global retinocortical signal transfer efficiency revealed a novel control mechanism resulting from the collective resonance of all thalamic relay neurons. We show here that the transfer efficiency of sensory input transmission depends on three key features: i) the number of thalamocortical cells involved in the many-to-one convergence from thalamus to cortex, ii) the statistics of the corticothalamic synaptic bombardment and iii) the level of correlation imposed between converging thalamic relay cells. In particular, our results demonstrate counterintuitively that the retinocortical signal transfer efficiency increases when the level of correlation across thalamic cells decreases. …”
19. A model for focal seizure onset, propagation, evolution, and progression (Liou et al 2020)
We developed a neural network model that can account for major elements common to human focal seizures. These include the tonic-clonic transition, slow advance of clinical semiology and corresponding seizure territory expansion, widespread EEG synchronization, and slowing of the ictal rhythm as the seizure approaches termination. These were reproduced by incorporating usage-dependent exhaustion of inhibition in an adaptive neural network that receives global feedback inhibition in addition to local recurrent projections. Our model proposes mechanisms that may underline common EEG seizure onset patterns and status epilepticus, and postulates a role for synaptic plasticity in the emergence of epileptic foci. Complex patterns of seizure activity and bi- stable seizure end-points arise when stochastic noise is included. With the rapid advancement of clinical and experimental tools, we believe that this model can provide a roadmap and potentially an in silico testbed for future explorations of seizure mechanisms and clinical therapies.
20. A model of antennal lobe of bee (Chen JY et al. 2015)
" ... Here we use calcium imaging to reveal how responses across antennal lobe projection neurons change after association of an input odor with appetitive reinforcement. After appetitive conditioning to 1-hexanol, the representation of an odor mixture containing 1-hexanol becomes more similar to this odor and less similar to the background odor acetophenone. We then apply computational modeling to investigate how changes in synaptic connectivity can account for the observed plasticity. Our study suggests that experience-dependent modulation of inhibitory interactions in the antennal lobe aids perception of salient odor components mixed with behaviorally irrelevant background odors."
21. A model of the femur-tibia control system in stick insects (Stein et al. 2008)
We studied the femur-tibia joint control system of the insect leg, and its switch between resistance reflex in posture control and "active reaction" in walking. The "active reaction" is basically a reversal of the resistance reflex. Both responses are elicited by the same sensory input and the same neuronal network (the femur-tibia network). The femur-tibia network was modeled by fitting the responses of model neurons to those obtained in animals. Each implemented neuron has a physiological counterpart. The strengths of 16 interneuronal pathways that integrate sensory input were then assigned three different values and varied independently, generating a database of more than 43 million network variants. The uploaded version contains the model that best represented the resistance reflex. Please see the README for more help. We demonstrate that the combinatorial code of interneuronal pathways determines motor output. A switch between different behaviors such as standing to walking can thus be achieved by altering the strengths of selected sensory integration pathways.
22. A model of the temporal pattern generator of C. elegans egg-laying behavior (Zhang et. al 2010)
"... We suggest that the HSN neuron is the executive neuron driving egg-laying events. We propose that the VC neurons act as "single egg counters" that inhibit HSN activity for short periods in response to individual egg-laying events. We further propose that the uv1 neuroendocrine cells are "cluster counters", which inhibit HSN activity for longer periods and are responsible for the time constant of the inactive phase. Together they form an integrated circuit that drives the clustered egg-laying pattern. ..."
23. A Moth MGC Model-A HH network with quantitative rate reduction (Buckley & Nowotny 2011)
We provide the model used in Buckley & Nowotny (2011). It consists of a network of Hodgkin Huxley neurons coupled by slow GABA_B synapses which is run alongside a quantitative reduction described in the associated paper.
24. A multilayer cortical model to study seizure propagation across microdomains (Basu et al. 2015)
A realistic neural network was used to simulate a region of neocortex to obtain extracellular LFPs from ‘virtual micro-electrodes’ and produce test data for comparison with multisite microelectrode recordings. A model was implemented in the GENESIS neurosimulator. A simulated region of cortex was represented by layers 2/3, 5/6 (interneurons and pyramidal cells) and layer 4 stelate cells, spaced at 25 µm in each horizontal direction. Pyramidal cells received AMPA and NMDA inputs from neighboring cells at the basal and apical dendrites. The LFP data was generated by simulating 16-site electrode array with the help of ‘efield’ objects arranged at the predetermined positions with respect to the surface of the simulated network. The LFP for the model is derived from a weighted average of the current sources summed over all cellular compartments. Cell models were taken from from Traub et al. (2005) J Neurophysiol 93(4):2194-232.
25. A network model of tail withdrawal in Aplysia (White et al 1993)
The contributions of monosynaptic and polysynaptic circuitry to the tail-withdrawal reflex in the marine mollusk Aplysia californica were assessed by the use of physiologically based neural network models. Effects of monosynaptic circuitry were examined by the use of a two-layer network model with four sensory neurons in the input layer and one motor neuron in the output layer. Results of these simulations indicated that the monosynaptic circuit could not account fully for long-duration responses of tail motor neurons elicited by tail stimulation. A three-layer network model was constructed by interposing a layer of two excitatory interneurons between the input and output layers of the two-layer network model. The three-layer model could account for long-duration responses in motor neurons. Sensory neurons are a known site of plasticity in Aplysia. Synaptic plasticity at more than one locus modified dramatically the input-output relationship of the three-layer network model. This feature gave the model redundancy in its plastic properties and points to the possibility of distributed memory in the circuitry mediating withdrawal reflexes in Aplysia. Please see paper for more results and details.
26. A network model of the vertebrate retina (Publio et al. 2009)
In this work, we use a minimal conductance-based model of the ON rod pathways in the vertebrate retina to study the effects of electrical synaptic coupling via gap junctions among rods and among AII amacrine cells on the dynamic range of the retina. The model is also used to study the effects of the maximum conductance of rod hyperpolarization activated current Ih on the dynamic range of the retina, allowing a study of the interrelations between this intrinsic membrane parameter with those two retina connectivity characteristics.
27. A network of AOB mitral cells that produces infra-slow bursting (Zylbertal et al. 2017)
Infra-slow rhythmic neuronal activity with very long (> 10 s) period duration was described in many brain areas but little is known about the role of this activity and the mechanisms that produce it. Here we combine experimental and computational methods to show that synchronous infra-slow bursting activity in mitral cells of the mouse accessory olfactory bulb (AOB) emerges from interplay between intracellular dynamics and network connectivity. In this novel mechanism, slow intracellular Na+ dynamics endow AOB mitral cells with a weak tendency to burst, which is further enhanced and stabilized by chemical and electrical synapses between them. Combined with the unique topology of the AOB network, infra-slow bursting enables integration and binding of multiple chemosensory stimuli over prolonged time scale. The example protocol simulates a two-glomeruli network with a single shared cell. Although each glomerulus is stimulated at a different time point, the activity of the entire population becomes synchronous (see paper Fig. 8)
28. A simulation method for the firing sequences of motor units (Jiang et al 2006)
" ... a novel model based on the Hodgkin–Huxley (HH) system is proposed, which has the ability to simulate the complex neurodynamics of the firing sequences of motor neurons. The model is presented at the cellular level and network level, and some simulation results from a simple 3-neuron network are presented to demonstrate its applications." See paper for more and details.
29. A single column thalamocortical network model (Traub et al 2005)
To better understand population phenomena in thalamocortical neuronal ensembles, we have constructed a preliminary network model with 3,560 multicompartment neurons (containing soma, branching dendrites, and a portion of axon). Types of neurons included superficial pyramids (with regular spiking [RS] and fast rhythmic bursting [FRB] firing behaviors); RS spiny stellates; fast spiking (FS) interneurons, with basket-type and axoaxonic types of connectivity, and located in superficial and deep cortical layers; low threshold spiking (LTS) interneurons, that contacted principal cell dendrites; deep pyramids, that could have RS or intrinsic bursting (IB) firing behaviors, and endowed either with non-tufted apical dendrites or with long tufted apical dendrites; thalamocortical relay (TCR) cells; and nucleus reticularis (nRT) cells. To the extent possible, both electrophysiology and synaptic connectivity were based on published data, although many arbitrary choices were necessary.
30. A spatial model of the intermediate superior colliculus (Moren et. al. 2013)
A spatial model of the intermediate superior colliculus. It reproduces the collicular saccade-generating output profile from NMDA receptor-driven burst neurons, shaped by integrative inhibitory feedback from spreading buildup neuron activity. The model is consistent with the view that collicular activity directly shapes the temporal profile of saccadic eye movements. We use the Adaptive exponential integrate and fire neuron model, augmented with an NMDA-like membrane potential-dependent receptor. In addition, we use a synthetic spike integrator model as a stand-in for a spike-integrator circuit in the reticular formation. NOTE: We use a couple of custom neuron models, so the supplied model file includes an entire version of NEST. I also include a patch that applies to a clean version of the simulator (see the doc/README).
31. A spiking model of cortical broadcast and competition (Shanahan 2008)
"This paper presents a computer model of cortical broadcast and competition based on spiking neurons and inspired by the hypothesis of a global neuronal workspace underlying conscious information processing in the human brain. In the model, the hypothesised workspace is realised by a collection of recurrently interconnected regions capable of sustaining and disseminating a reverberating spatial pattern of activation. ..."
32. A spiking neural network model of model-free reinforcement learning (Nakano et al 2015)
"Spiking neural networks provide a theoretically grounded means to test computational hypotheses on neurally plausible algorithms of reinforcement learning through numerical simulation. ... In this work, we use a spiking neural network model to approximate the free energy of a restricted Boltzmann machine and apply it to the solution of PORL (partially observable reinforcement learning) problems with high-dimensional observations. ... The way spiking neural networks handle PORL problems may provide a glimpse into the underlying laws of neural information processing which can only be discovered through such a top-down approach. "
33. A spiking neural network model of the Lateral Geniculate Nucleus (Sen-Bhattacharya et al 2017)
Using Izhikevich's spiking neuron models, to build a network with a biologically informed synaptic layout emulating the Lateral Geniculate Nucleus.
34. A spiking NN for amplification of feature-selectivity with specific connectivity (Sadeh et al 2015)
The model simulates large-scale inhibition-dominated spiking networks with different degrees of recurrent specific connectivity. It shows how feature-specific connectivity leads to a linear amplification of feedforward tuning, as reported in recent electrophysiological single-neuron recordings in rodent neocortex. Moreover, feature-specific connectivity leads to the emergence of feature-selective reverberating activity, and entails pattern completion in network responses.
35. A two networks model of connectivity-dependent oscillatory activity (Avella OJ et al. 2014)
Activity in a cortical network may express a single oscillation frequency, alternate between two or more distinct frequencies, or continually express multiple frequencies. In addition, oscillation amplitude may fluctuate over time. Interactions between oscillatory networks may contribute, but their effects are poorly known. Here, we created a two model networks, one generating on its own a relatively slow frequency (slow network) and one generating a fast frequency (fast network). We chose the slow or the fast network as source network projecting feed-forward connections to the other, or target network, and systematically investigated how type and strength of inter-network connections affected target network activity. Our results strongly depended on three factors: the type of the relevant (main) connection, its strength and the amount of source synapses. For high inter-network connection strengths, we found that the source network could completely impose its rhythm on the target network. Interestingly, the slow network was more effective at imposing its rhythm on the fast network than the other way around. The strongest entrainment occurred when excitatory cells of the slow network projected to excitatory or inhibitory cells of the fast network. Just as observed in rat activity at the prefrontal cortex satisfies the behavior described above, such that together, our results suggest that input from other oscillating networks may markedly alter a network’s frequency spectrum and may partly be responsible for the rich repertoire of temporal oscillation patterns observed in the brain.
36. A two-layer biophysical olfactory bulb model of cholinergic neuromodulation (Li and Cleland 2013)
This is a two-layer biophysical olfactory bulb (OB) network model to study cholinergic neuromodulation. Simulations show that nicotinic receptor activation sharpens mitral cell receptive field, while muscarinic receptor activation enhances network synchrony and gamma oscillations. This general model suggests that the roles of nicotinic and muscarinic receptors in OB are both distinct and complementary to one another, together regulating the effects of ascending cholinergic inputs on olfactory bulb transformations.
37. A unified thalamic model of multiple distinct oscillations (Li, Henriquez and Fröhlich 2017)
We present a unified model of the thalamus that is capable of independently generating multiple distinct oscillations (delta, spindle, alpha and gamma oscillations) under different levels of acetylcholine (ACh) and norepinephrine (NE) modulation corresponding to different physiological conditions (deep sleep, light sleep, relaxed wakefulness and attention). The model also shows that entrainment of thalamic oscillations is state-dependent.
38. Acetylcholine-modulated plasticity in reward-driven navigation (Zannone et al 2018)
"Neuromodulation plays a fundamental role in the acquisition of new behaviours. In previous experimental work, we showed that acetylcholine biases hippocampal synaptic plasticity towards depression, and the subsequent application of dopamine can retroactively convert depression into potentiation. We also demonstrated that incorporating this sequentially neuromodulated Spike- Timing-Dependent Plasticity (STDP) rule in a network model of navigation yields effective learning of changing reward locations. Here, we employ computational modelling to further characterize the effects of cholinergic depression on behaviour. We find that acetylcholine, by allowing learning from negative outcomes, enhances exploration over the action space. We show that this results in a variety of effects, depending on the structure of the model, the environment and the task. Interestingly, sequentially neuromodulated STDP also yields flexible learning, surpassing the performance of other reward-modulated plasticity rules."
39. ACh modulation in olfactory bulb and piriform cortex (de Almeida et al. 2013;Devore S, et al. 2014)
This matlab code was used in the papers de Almeida, Idiart and Linster, (2013), Devore S, de Almeida L, Linster C (2014) . This work uses a computational model of the OB and PC and their common cholinergic inputs to investigate how bulbar cholinergic modulation affects cortical odor processing.
40. ACnet23 primary auditory cortex model (Beeman et al 2019)
These scripts were used to model a patch of layer 2/3 primary auditory cortex, making use of the the improvements to PGENESIS by Crone, et al. (2019). This single layer model contains a 48 x 48 grid of pyramidal cells (PCs) and a 24 x 24 grid of basket cells (BCs). The reduced PC models have 17 compartments with dimensions and passive properties that were fit to human cortical PC reconstructions. This parallel version of the simulation was used by Beeman, et al. (2019) to understand the effects of inhibition of PCs by BCs on auditory evoked potentials.
41. Activity constraints on stable neuronal or network parameters (Olypher and Calabrese 2007)
"In this study, we developed a general description of parameter combinations for which specified characteristics of neuronal or network activity are constant. Our approach is based on the implicit function theorem and is applicable to activity characteristics that smoothly depend on parameters. Such smoothness is often intrinsic to neuronal systems when they are in stable functional states. The conclusions about how parameters compensate each other, developed in this study, can thus be used even without regard to the specific mathematical model describing a particular neuron or neuronal network. ..."
42. Activity patterns in a subthalamopallidal network of the basal ganglia model (Terman et al 2002)
"Based on recent experimental data, we have developed a conductance-based computational network model of the subthalamic nucleus and the external segment of the globus pallidus in the indirect pathway of the basal ganglia. Computer simulations and analysis of this model illuminate the roles of the coupling architecture of the network, and associated synaptic conductances, in modulating the activity patterns displayed by this network. Depending on the relationships of these coupling parameters, the network can support three general classes of sustained firing patterns: clustering, propagating waves, and repetitive spiking that may show little regularity or correlation. ...". Terman's XPP code and a partial implementation by Taylor Malone in NEURON and python are included.
43. Adaptive robotic control driven by a versatile spiking cerebellar network (Casellato et al. 2014)
" ... We have coupled a realistic cerebellar spiking neural network (SNN) with a real robot and challenged it in multiple diverse sensorimotor tasks. ..."
44. Alpha rhythm in vitro visual cortex (Traub et al 2020)
The paper describes an experimental model of the alpha rhythm generated by layer 4 pyramidal neurons in a visual cortex slice. The simulation model is derived from that of Traub et al. (2005) J Neurophysiol, developed for thalamocortical oscillations.
45. An attractor network model of grid cells and theta-nested gamma oscillations (Pastoll et al 2013)
A two population spiking continuous attractor model of grid cells. This model combines the attractor dynamics with theta-nested gamma oscillatory activity. It reproduces the behavioural response of grid cells (grid fields) in medial entorhinal cortex, while at the same time allowing for nested gamma oscillations of post-synaptic currents.
46. An electrophysiological model of GABAergic double bouquet cells (Chrysanthidis et al. 2019)
We present an electrophysiological model of double bouquet cells (DBCs) and integrate them into an established cortical columnar microcircuit model that implements a BCPNN (Bayesian Confidence Propagation Neural Network) learning rule. The proposed architecture effectively solves the problem of duplexed learning of inhibition and excitation by replacing recurrent inhibition between pyramidal cells in functional columns of different stimulus selectivity with a plastic disynaptic pathway. The introduction of DBCs improves the biological plausibility of our model, without affecting the model's spiking activity, basic operation, and learning abilities.
47. Asynchronous irregular and up/down states in excitatory and inhibitory NNs (Destexhe 2009)
"Randomly-connected networks of integrate-and-fire (IF) neurons are known to display asynchronous irregular (AI) activity states, which resemble the discharge activity recorded in the cerebral cortex of awake animals. ... Here, we investigate the occurrence of AI states in networks of nonlinear IF neurons, such as the adaptive exponential IF (Brette-Gerstner-Izhikevich) model. This model can display intrinsic properties such as low-threshold spike (LTS), regular spiking (RS) or fast-spiking (FS). We successively investigate the oscillatory and AI dynamics of thalamic, cortical and thalamocortical networks using such models. ..."
48. Auditory cortex layer IV network model (Beeman 2013)
"... The primary objective of this modeling study was to determine the effects of axonal conduction velocity (often neglected, but significant), as well as synaptic time constants, on the ability of such a network to create and propagate cortical waves. ... The model is also being used to study the interaction between single and two-tone input and normal background activity, and the effects of synaptic depression from thalamic inputs. The simulation scripts have the additional purpose of serving as tutorial examples for the construction of cortical networks with GENESIS. The present model has fostered the development of the G-3 Python network analysis and visualization tools used in this study... It is my hope that this short tutorial and the example simulation scripts can provide a head start for a graduate student or postdoc who is beginning a cortical modeling project. "
49. Axonal gap junctions produce fast oscillations in cerebellar Purkinje cells (Traub et al. 2008)
Examines how electrical coupling between proximal axons produces fast oscillations in cerebellar Purkinje cells. Traub RD, Middleton SJ, Knopfel T, Whittington MA (2008) Model of very fast (>75 Hz) network oscillations generated by electrical coupling between the proximal axons of cerebellar Purkinje cells. European Journal of Neuroscience.
50. Basal ganglia network model of subthalamic deep brain stimulation (Hahn and McIntyre 2010)
Basal ganglia network model of parkinsonian activity and subthalamic deep brain stimulation in non-human primates from the article Instructions are provided in the README.txt file. Contact hahnp@ccf.org if you have any questions about the implementation of the model. Please include "ModelDB - BGnet" in the subject heading.
51. Basal ganglia-thalamic network model for deep brain stimulation (So et al. 2012)
This is a model of the basal ganglia-thalamic network, modified from the Rubin and Terman model (High frequency stimulation of the Subthalamic Nucleus, Rubin and Terman 2004). We subsequently used this model to investigate the effectiveness of STN and GPi DBS as well as lesion when various proportions of local cells and fibers of passage were activated or silenced. The BG network exhibited characteristics consistent with published experimental data, both on the level of single cells and on the network level. Perhaps most notably, and in contrast to the original RT model, the changes in the thalamic error index with changes in the DBS frequency matched well the changes in clinical symptoms with changes in DBS frequency.
52. Basis for temporal filters in the cerebellar granular layer (Roessert et al. 2015)
This contains the models, functions and resulting data as used in: Roessert C, Dean P, Porrill J. At the Edge of Chaos: How Cerebellar Granular Layer Network Dynamics Can Provide the Basis for Temporal Filters. It is based on code used for Yamazaki T, Tanaka S (2005) Neural modeling of an internal clock. Neural Comput 17:1032-58
53. Biologically Constrained Basal Ganglia model (BCBG model) (Lienard, Girard 2014)
We studied the physiology and function of the basal ganglia through the design of mean-field models of the whole basal ganglia. The parameterizations are optimized with multi-objective evolutionary algorithm to respect best a collection of numerous anatomical data and electrophysiological data. The main outcomes of our study are: • The strength of the GPe to GPi/SNr connection does not support opposed activities in the GPe and GPi/SNr. • STN and MSN target more the GPe than the GPi/SNr. • Selection arises from the structure of the basal ganglia, without properly segregated direct and indirect pathways and without specific inputs from pyramidal tract neurons of the cortex. Selection is enhanced when the projection from GPe to GPi/SNr has a diffuse pattern.
54. Biophysical model for field potentials of networks of I&F neurons (beim Graben & Serafim 2013)
"... Starting from a reduced three-compartment model of a single pyramidal neuron, we derive an observation model for dendritic dipole currents in extracellular space and thereby for the dendritic field potential (DFP) that contributes to the local field potential (LFP) of a neural population. ... Our reduced three-compartment scheme allows to derive networks of leaky integrate-and-fire (LIF) models, which facilitates comparison with existing neural network and observation models. ..."
55. Biophysically realistic neural modeling of the MEG mu rhythm (Jones et al. 2009)
"Variations in cortical oscillations in the alpha (7–14 Hz) and beta (15–29 Hz) range have been correlated with attention, working memory, and stimulus detection. The mu rhythm recorded with magnetoencephalography (MEG) is a prominent oscillation generated by Rolandic cortex containing alpha and beta bands. Despite its prominence, the neural mechanisms regulating mu are unknown. We characterized the ongoing MEG mu rhythm from a localized source in the finger representation of primary somatosensory (SI) cortex. Subjects showed variation in the relative expression of mu-alpha or mu-beta, which were nonoverlapping for roughly 50% of their respective durations on single trials. To delineate the origins of this rhythm, a biophysically principled computational neural model of SI was developed, with distinct laminae, inhibitory and excitatory neurons, and feedforward (FF, representative of lemniscal thalamic drive) and feedback (FB, representative of higher-order cortical drive or input from nonlemniscal thalamic nuclei) inputs defined by the laminar location of their postsynaptic effects. ..."
56. Broadening of activity with flow across neural structures (Lytton et al. 2008)
"Synfire chains have long been suggested as a substrate for perception and information processing in the nervous system. However, embedding activation chains in a densely connected nervous matrix risks spread of signal that will obscure or obliterate the message. We used computer modeling and physiological measurements in rat hippocampus to assess this problem of activity broadening. We simulated a series of neural modules with feedforward propagation and random connectivity within each module and from one module to the next. ..."
57. Burst induced synaptic plasticity in Apysia sensorimotor neurons (Phares et al 2003)
The Aplysia sensorimotor synapse is a key site of plasticity for several simple forms of learning. Intracellular stimulation of sensory neurons to fire a burst of action potentials at 10 Hz for 1 sec led to significant homosynaptic depression of postsynaptic responses. During the burst, the steady-state depressed phase of the postsynaptic response, which was only 20% of the initial EPSP of the burst, still contributed to firing the motor neuron. To explore the functional contribution of transient homosynaptic depression to the response of the motor neuron, computer simulations of the sensorimotor synapse with and without depression were compared. Depression allowed the motor neuron to produce graded responses over a wide range of presynaptic input strength. Thus, synaptic depression increased the dynamic range of the sensorimotor synapse and can, in principle, have a profound effect on information processing. Please see paper for results and details.
58. Bursting and oscillations in RD1 Retina driven by AII Amacrine Neuron (Choi et al. 2014)
"In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. ..."
59. Bursting respiratory net: clustered architecture gives large phase diff`s (Fietkiewicz et al 2011)
Using a previous model of respiratory rhythm generation, we modified the network architecture such that cells can be segregated into two clusters. Cells within a given cluster burst with smaller phase differences than do cells from different clusters. This may explain the large phase differences seen experimentally, as reported in the paper.
60. Ca+/HCN channel-dependent persistent activity in multiscale model of neocortex (Neymotin et al 2016)
"Neuronal persistent activity has been primarily assessed in terms of electrical mechanisms, without attention to the complex array of molecular events that also control cell excitability. We developed a multiscale neocortical model proceeding from the molecular to the network level to assess the contributions of calcium regulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in providing additional and complementary support of continuing activation in the network. ..."
61. CA1 network model for place cell dynamics (Turi et al 2019)
Biophysical model of CA1 hippocampal region. The model simulates place cells/fields and explores the place cell dynamics as function of VIP+ interneurons.
62. CA1 network model: interneuron contributions to epileptic deficits (Shuman et al 2019)
Temporal lobe epilepsy causes significant cognitive deficits in both humans and rodents, yet the specific circuit mechanisms underlying these deficits remain unknown. There are profound and selective interneuron death and axonal reorganization within the hippocampus of both humans and animal models of temporal lobe epilepsy. To assess the specific contribution of these mechanisms on spatial coding, we developed a biophysically constrained network model of the CA1 region that consists of different subtypes of interneurons. More specifically, our network consists of 150 cells, 130 excitatory pyramidal cells and 20 interneurons (Fig. 1A). To simulate place cell formation in the network model, we generated grid cell and place cell inputs from the Entorhinal Cortex (ECLIII) and CA3 regions, respectively, activated in a realistic manner as observed when an animal transverses a linear track. Realistic place fields emerged in a subpopulation of pyramidal cells (40-50%), in which similar EC and CA3 grid cell inputs converged onto distal/proximal apical and basal dendrites. The tuning properties of these cells are very similar to the ones observed experimentally in awake, behaving animals To examine the role of interneuron death and axonal reorganization in the formation and/or tuning properties of place fields we selectively varied the contribution of each interneuron type and desynchronized the two excitatory inputs. We found that desynchronized inputs were critical in reproducing the experimental data, namely the profound reduction in place cell numbers, stability and information content. These results demonstrate that the desynchronized firing of hippocampal neuronal populations contributes to poor spatial processing in epileptic mice, during behavior. Given the lack of experimental data on the selective contributions of interneuron death and axonal reorganization in spatial memory, our model findings predict the mechanistic effects of these alterations at the cellular and network levels.
63. CA1 pyr cell: Inhibitory modulation of spatial selectivity+phase precession (Grienberger et al 2017)
Spatially uniform synaptic inhibition enhances spatial selectivity and temporal coding in CA1 place cells by suppressing broad out-of-field excitation.
64. CA1 pyramidal cell: reconstructed axonal arbor and failures at weak gap junctions (Vladimirov 2011)
Model of pyramidal CA1 cells connected by gap junctions in their axons. Cell geometry is based on anatomical reconstruction of rat CA1 cell (NeuroMorpho.Org ID: NMO_00927) with long axonal arbor. Model init_2cells.hoc shows failures of second spike propagation in a spike doublet, depending on conductance of an axonal gap junction. Model init_ring.hoc shows that spike failure result in reentrant oscillations of a spike in a loop of axons connected by gap junctions, where one gap junction is weak. The paper shows that in random networks of axons connected by gap junctions, oscillations are driven by single pacemaker loop of axons. The shortest loop, around which a spike can travel, is the most likely pacemaker. This principle allows us to predict the frequency of oscillations from network connectivity and visa versa. We propose that this type of oscillations corresponds to so-called fast ripples in epileptic hippocampus.
65. CA1 pyramidal cells, basket cells, ripples (Malerba et al 2016)
Model of CA1 pyramidal layer Ripple activity, triggered when receiving current input (to represent CA3 sharp-waves). Cells are Adaptive-Exponential Integrate and Fire neurons, receiving independent OU noise.
66. CA1 pyramidal neuron network model (Ferguson et al 2015)
From the paper: Figure 4 (1000 cell network) is reproduced by running this brian code. The raster plot and one of the excitatory cell voltage is produced.
67. Ca2+-activated I_CAN and synaptic depression promotes network-dependent oscil. (Rubin et al. 2009)
"... the preBotzinger complex... we present and analyze a mathematical model demonstrating an unconventional mechanism of rhythm generation in which glutamatergic synapses and the short-term depression of excitatory transmission play key rhythmogenic roles. Recurrent synaptic excitation triggers postsynaptic Ca2+- activated nonspecific cation current (ICAN) to initiate a network-wide burst. Robust depolarization due to ICAN also causes voltage-dependent spike inactivation, which diminishes recurrent excitation and thus attenuates postsynaptic Ca2+ accumulation. ..."
68. CA3 Network Model of Epileptic Activity (Sanjay et. al, 2015)
This computational study investigates how a CA3 neuronal network consisting of pyramidal cells, basket cells and OLM interneurons becomes epileptic when dendritic inhibition to pyramidal cells is impaired due to the dysfunction of OLM interneurons. After standardizing the baseline activity (theta-modulated gamma oscillations), systematic changes are made in the connectivities between the neurons, as a result of step-wise impairment of dendritic inhibition.
69. Cancelling redundant input in ELL pyramidal cells (Bol et al. 2011)
The paper investigates the property of the electrosensory lateral line lobe (ELL) of the brain of weakly electric fish to cancel predictable stimuli. Electroreceptors on the skin encode all signals in their firing activity, but superficial pyramidal (SP) cells in the ELL that receive this feedforward input do not respond to constant sinusoidal signals. This cancellation putatively occurs using a network of feedback delay lines and burst-induced synaptic plasticity between the delay lines and the SP cell that learns to cancel the redundant input. Biologically, the delay lines are parallel fibres from cerebellar-like granule cells in the eminentia granularis posterior. A model of this network (e.g. electroreceptors, SP cells, delay lines and burst-induced plasticity) was constructed to test whether the current knowledge of how the network operates is sufficient to cancel redundant stimuli.
70. Cell splitting in neural networks extends strong scaling (Hines et al. 2008)
Neuron tree topology equations can be split into two subtrees and solved on different processors with no change in accuracy, stability, or computational effort; communication costs involve only sending and receiving two double precision values by each subtree at each time step. Application of the cell splitting method to two published network models exhibits good runtime scaling on twice as many processors as could be effectively used with whole-cell balancing.
71. Cerebellar cortex oscil. robustness from Golgi cell gap jncs (Simoes de Souza and De Schutter 2011)
" ... Previous one-dimensional network modeling of the cerebellar granular layer has been successfully linked with a range of cerebellar cortex oscillations observed in vivo. However, the recent discovery of gap junctions between Golgi cells (GoCs), which may cause oscillations by themselves, has raised the question of how gap-junction coupling affects GoC and granular-layer oscillations. To investigate this question, we developed a novel two-dimensional computational model of the GoC-granule cell (GC) circuit with and without gap junctions between GoCs. ..."
72. Cerebellar gain and timing control model (Yamazaki & Tanaka 2007)(Yamazaki & Nagao 2012)
This paper proposes a hypothetical computational mechanism for unified gain and timing control in the cerebellum. The hypothesis is justified by computer simulations of a large-scale spiking network model of the cerebellum.
73. Cerebellar granular layer (Maex and De Schutter 1998)
Circuit model of the granular layer representing a one-dimensional array of single-compartmental granule cells (grcs) and Golgi cells (Gocs). This paper examines the effects of feedback inhibition (grc -> Goc -> grc) versus feedforward inhibition (mossy fibre -> Goc -> grc) on synchronization and oscillatory behaviour.
74. Changes of ionic concentrations during seizure transitions (Gentiletti et al. 2016)
"... In order to investigate the respective roles of synaptic interactions and nonsynaptic mechanisms in seizure transitions, we developed a computational model of hippocampal cells, involving the extracellular space, realistic dynamics of Na+, K+, Ca2+ and Cl - ions, glial uptake and extracellular diffusion mechanisms. We show that the network behavior with fixed ionic concentrations may be quite different from the neurons’ behavior when more detailed modeling of ionic dynamics is included. In particular, we show that in the extended model strong discharge of inhibitory interneurons may result in long lasting accumulation of extracellular K+, which sustains the depolarization of the principal cells and causes their pathological discharges. ..."
75. Classic model of the Tritonia Swim CPG (Getting, 1989)
Classic model developed by Petter Getting of the 3-cell core CPG (DSI, C2, and VSI-B) mediating escape swimming in Tritonia diomedea. Cells use a hybrid integrate-and-fire scheme pioneered by Peter Getting. Each model cell is reconstructed from extensive physiological measurements to precisely mimic I-F curves, synaptic waveforms, and functional connectivity. **However, continued physiological measurements show that Getting may have inadvertently incorporated modulatory and or polysynaptic effects -- the properties of this model do *not* match physiological measurements in rested preparations.** This simulation reconstructs the Getting model as reported in: Getting (1989) 'Reconstruction of small neural networks' In Methods in Neural Modeling, 1st ed, p. 171-196. See also, an earlier version of this model reported in Getting (1983). Every attempt has been made to replicate the 1989 model as precisely as possible.
76. Coding of stimulus frequency by latency in thalamic networks (Golomb et al 2005)
The paper presents models of the rat vibrissa processing system including the posterior medial (POm) thalamus, ventroposterior medial (VPm) thalamus, and GABAB- mediated feedback inhibition from the reticular thalamic (Rt) nucleus. A clear match between the experimentally measured spike-rates and the numerically calculated rates for the full model occurs when VPm thalamus receives stronger brainstem input and weaker GABAB-mediated inhibition than POm thalamus.
77. Collection of simulated data from a thalamocortical network model (Glabska, Chintaluri, Wojcik 2017)
"A major challenge in experimental data analysis is the validation of analytical methods in a fully controlled scenario where the justification of the interpretation can be made directly and not just by plausibility. ... One solution is to use simulations of realistic models to generate ground truth data. In neuroscience, creating such data requires plausible models of neural activity, access to high performance computers, expertise and time to prepare and run the simulations, and to process the output. To facilitate such validation tests of analytical methods we provide rich data sets including intracellular voltage traces, transmembrane currents, morphologies, and spike times. ... The data were generated using the largest publicly available multicompartmental model of thalamocortical network (Traub et al. 2005), with activity evoked by different thalamic stimuli."
78. Competing oscillator 5-cell circuit and Parameterscape plotting (Gutierrez et al. 2013)
Our 5-cell model consists of competing fast and slow oscillators connected to a hub neuron with electrical and inhibitory synapses. Motivated by the Stomatogastric Ganglion (STG) circuit in the crab, we explored the patterns of coordination in the network as a function of the electrical coupling and inhibitory synapse strengths with the help of a novel visualization method that we call the "Parameterscape." The code submitted here will allow you to run circuit simulations and to produce a Parameterscape with the results.
79. Competition for AP initiation sites in a circuit controlling simple learning (Cruz et al. 2007)
"The spatial and temporal patterns of action potential initiations were studied in a behaving leech preparation to determine the basis of increased firing that accompanies sensitization, a form of non-associative learning requiring the S-interneurons. ... The S-interneurons, one in each ganglion and linked by electrical synapses with both neighbors to form a chain, are interposed between sensory and motor neurons. ... the single site with the largest initiation rate, the S-cell in the stimulated segment, suppressed initiations in adjacent ganglia. Experiments showed this was both because (1) it received the earliest, greatest input and (2) the delayed synaptic input to the adjacent S-cells coincided with the action potential refractory period. A compartmental model of the S-cell and its inputs showed that a simple, intrinsic mechanism of inexcitability after each action potential may account for suppression of impulse initiations. Thus, a non-synaptic competition between neurons alters synaptic integration in the chain. In one mode, inputs to different sites sum independently, whereas in another, synaptic input to a single site precisely specifies the overall pattern of activity."
80. Competition model of pheromone ratio detection (Zavada et al. 2011)
For some closely related sympatric moth species, recognizing a specific pheromone component concentration ratio is essential for mating success. We propose and test a minimalist competition-based feed-forward neuronal model capable of detecting a certain ratio of pheromone components independently of overall concentration. This model represents an elementary recognition unit for binary mixtures which we propose is entirely contained in the macroglomerular complex (MGC) of the male moth. A set of such units, along with projection neurons (PNs), can provide the input to higher brain centres. We found that (1) accuracy is mainly achieved by maintaining a certain ratio of connection strengths between olfactory receptor neurons (ORN) and local neurons (LN), much less by properties of the interconnections between the competing LNs proper. (2) successful ratio recognition is achieved using latency-to-first-spike in the LN populations which. (3) longer durations of the competition process between LNs did not result in higher recognition accuracy.
81. Complex dynamics: reproducing Golgi cell electroresponsiveness (Geminiani et al 2018, 2019ab)
Excerpts from three papers abstracts: "Brain neurons exhibit complex electroresponsive properties – including intrinsic subthreshold oscillations and pacemaking, resonance and phase-reset – which are thought to play a critical role in controlling neural network dynamics. Although these properties emerge from detailed representations of molecular-level mechanisms in “realistic” models, they cannot usually be generated by simplified neuronal models (although these may show spike-frequency adaptation and bursting). We report here that this whole set of properties can be generated by the extended generalized leaky integrate-and-fire (E-GLIF) neuron model. ..." "... In order to reproduce these properties in single-point neuron models, we have optimized the Extended-Generalized Leaky Integrate and Fire (E-GLIF) neuron through a multi-objective gradient-based algorithm targeting the desired input–output relationships. ..." " ... In order to investigate how single neuron dynamics and geometrical modular connectivity affect cerebellar processing, we have built an olivocerebellar Spiking Neural Network (SNN) based on a novel simplification algorithm for single point models (Extended Generalized Leaky Integrate and Fire, EGLIF) capturing essential non-linear neuronal dynamics (e.g., pacemaking, bursting, adaptation, oscillation and resonance). ..."
82. Composite spiking network/neural field model of Parkinsons (Kerr et al 2013)
This code implements a composite model of Parkinson's disease (PD). The composite model consists of a leaky integrate-and-fire spiking neuronal network model being driven by output from a neural field model (instead of the more usual white noise drive). Three different sets of parameters were used for the field model: one with basal ganglia parameters based on data from healthy individuals, one based on data from individuals with PD, and one purely thalamocortical model. The aim of this model is to explore how the different dynamical patterns in each each of these field models affects the activity in the network model.
83. Computational analysis of NN activity and spatial reach of sharp wave-ripples (Canakci et al 2017)
Network oscillations of different frequencies, durations and amplitudes are hypothesized to coordinate information processing and transfer across brain areas. Among these oscillations, hippocampal sharp wave-ripple complexes (SPW-Rs) are one of the most prominent. SPW-Rs occurring in the hippocampus are suggested to play essential roles in memory consolidation as well as information transfer to the neocortex. To-date, most of the knowledge about SPW-Rs comes from experimental studies averaging responses from neuronal populations monitored by conventional microelectrodes. In this work, we investigate spatiotemporal characteristics of SPW-Rs and how microelectrode size and distance influence SPW-R recordings using a biophysical model of hippocampus. We also explore contributions from neuronal spikes and synaptic potentials to SPW-Rs based on two different types of network activity. Our study suggests that neuronal spikes from pyramidal cells contribute significantly to ripples while high amplitude sharp waves mainly arise from synaptic activity. Our simulations on spatial reach of SPW-Rs show that the amplitudes of sharp waves and ripples exhibit a steep decrease with distance from the network and this effect is more prominent for smaller area electrodes. Furthermore, the amplitude of the signal decreases strongly with increasing electrode surface area as a result of averaging. The relative decrease is more pronounced when the recording electrode is closer to the source of the activity. Through simulations of field potentials across a high-density microelectrode array, we demonstrate the importance of finding the ideal spatial resolution for capturing SPW-Rs with great sensitivity. Our work provides insights on contributions from spikes and synaptic potentials to SPW-Rs and describes the effect of measurement configuration on LFPs to guide experimental studies towards improved SPW-R recordings.
84. Computational aspects of feedback in neural circuits (Maass et al 2006)
It had previously been shown that generic cortical microcircuit models can perform complex real-time computations on continuous input streams, provided that these computations can be carried out with a rapidly fading memory. We investigate ... the computational capability of such circuits in the more realistic case where not only readout neurons, but in addition a few neurons within the circuit have been trained for specific tasks. This is essentially equivalent to the case where the output of trained readout neurons is fed back into the circuit. We show that this new model overcomes the limitation of a rapidly fading memory. In fact, we prove that in the idealized case without noise it can carry out any conceiv- able digital or analog computation on time-varying inputs. But even with noise the resulting computational model can perform a large class of biologically relevant real-time computations that require a non-fading memory. ... In particular we show that ... generic cortical microcircuits with feedback provide a new model for working memory that is consistent with a large set of biological constraints. See paper for more and details.
85. Computational Model of a Central Pattern Generator (Cataldo et al 2006)
The buccal ganglia of Aplysia contain a central pattern generator (CPG) that mediates rhythmic movements of the foregut during feeding. This CPG is a multifunctional circuit and generates at least two types of buccal motor patterns (BMPs), one that mediates ingestion (iBMP) and another that mediates rejection (rBMP). The present study used a computational approach to examine the ways in which an ensemble of identified cells and synaptic connections function as a CPG. Hodgkin-Huxley-type models were developed that mimicked the biophysical properties of these cells and synaptic connections. The results suggest that the currently identified ensemble of cells is inadequate to produce rhythmic neural activity and that several key elements of the CPG remain to be identified.
86. Computational model of the distributed representation of operant reward memory (Costa et al. 2020)
Operant reward learning of feeding behavior in Aplysia increases the frequency and regularity of biting, as well as biases buccal motor patterns (BMPs) toward ingestion-like BMPs (iBMPs). The engram underlying this memory comprises cells that are part of a central pattern generating (CPG) circuit and includes increases in the intrinsic excitability of identified cells B30, B51, B63, and B65, and increases in B63–B30 and B63–B65 electrical synaptic coupling. To examine the ways in which sites of plasticity (individually and in combination) contribute to memory expression, a model of the CPG was developed. The model included conductance-based descriptions of cells CBI-2, B4, B8, B20, B30, B31, B34, B40, B51, B52, B63, B64, and B65, and their synaptic connections. The model generated patterned activity that resembled physiological BMPs, and implementation of the engram reproduced increases in frequency, regularity, and bias. Combined enhancement of B30, B63, and B65 excitabilities increased BMP frequency and regularity, but not bias toward iBMPs. Individually, B30 increased regularity and bias, B51 increased bias, B63 increased frequency, and B65 decreased all three BMP features. Combined synaptic plasticity contributed primarily to regularity, but also to frequency and bias. B63–B30 coupling contributed to regularity and bias, and B63–B65 coupling contributed to all BMP features. Each site of plasticity altered multiple BMP features simultaneously. Moreover, plasticity loci exhibited mutual dependence and synergism. These results indicate that the memory for operant reward learning emerged from the combinatoric engagement of multiple sites of plasticity.
87. Computational Surgery (Lytton et al. 2011)
Figure 2 in Neocortical simulation for epilepsy surgery guidance: Localization and intervention, by William W. Lytton, Samuel A. Neymotin, Jason C. Wester, and Diego Contreras in Computational Surgery and Dual Training, Springer, 2011
88. Computer model of clonazepam`s effect in thalamic slice (Lytton 1997)
Demonstration of the effect of a minor pharmacological synaptic change at the network level. Clonazepam, a benzodiazepine, enhances inhibition but is paradoxically useful for certain types of seizures. This simulation shows how inhibition of inhibitory cells (the RE cells) produces this counter-intuitive effect.
89. Computing with neural synchrony (Brette 2012)
"... In a heterogeneous neural population, it appears that synchrony patterns represent structure or sensory invariants in stimuli, which can then be detected by postsynaptic neurons. The required neural circuitry can spontaneously emerge with spike-timing-dependent plasticity. Using examples in different sensory modalities, I show that this allows simple neural circuits to extract relevant information from realistic sensory stimuli, for example to identify a fluctuating odor in the presence of distractors. ..."
90. Conductance-based model of Layer-4 in the barrel cortex (Argaman et Golomb 2017)
Layer 4 in the mouse barrel cortex includes hundreds of inhibitory PV neurons and thousands of excitatory neurons. Despite this fact, its dynamical state is similar to a balanced state of large neuronal circuits.
91. Contribution of ATP-sensitive potassium channels in the neuronal network (Huang et al. 2009)
Epileptic seizures in diabetic hyperglycemia (DH) are not uncommon. This study aimed to determine the acute behavioral, pathological, and electrophysiological effects of status epilepticus (SE) on diabetic animals. ... We also used a simulation model to evaluate intracellular adenosine triphosphate (ATP) and neuroexcitability. ... In the simulation, increased intracellular ATP concentration promoted action potential firing. This finding that rats with DH had more brain damage after SE than rats without diabetes suggests the importance of intensively treating hyperglycemia and seizures in diabetic patients with epilepsy.
92. Convergence regulates synchronization-dependent AP transfer in feedforward NNs (Sailamul et al 2017)
We study how synchronization-dependent spike transfer can be affected by the structure of convergent feedforward wiring. We implemented computer simulations of model neural networks: a source and a target layer connected with different types of convergent wiring rules. In the Gaussian-Gaussian (GG) model, both the connection probability and the strength are given as Gaussian distribution as a function of spatial distance. In the Uniform-Constant (UC) and Uniform-Exponential (UE) models, the connection probability density is a uniform constant within a certain range, but the connection strength is set as a constant value or an exponentially decaying function, respectively. Then we examined how the spike transfer function is modulated under these conditions, while static or synchronized input patterns were introduced to simulate different levels of feedforward spike synchronization. We observed that the synchronization-dependent modulation of the transfer function appeared noticeably different for each convergence condition. The modulation of the spike transfer function was largest in the UC model, and smallest in the UE model. Our analysis showed that this difference was induced by the different spike weight distributions that was generated from convergent synapses in each model. Our results suggest that the structure of the feedforward convergence is a crucial factor for correlation-dependent spike control, thus must be considered important to understand the mechanism of information transfer in the brain.
93. Core respiratory network organization: Insights from optogenetics and modeling (Ausborn et al 2018)
"The circuit organization within the mammalian brainstem respiratory network, specifically within and between the pre-Bötzinger (pre-BötC) and Bötzinger (BötC) complexes, and the roles of these circuits in respiratory pattern generation are continuously debated. We address these issues with a combination of optogenetic experiments and modeling studies. We used transgenic mice expressing channelrhodopsin-2 under the VGAT-promoter to investigate perturbations of respiratory circuit activity by site-specific photostimulation of inhibitory neurons within the pre-BötC or BötC. The stimulation effects were dependent on the intensity and phase of the photostimulation. Specifically: (1) Low intensity (= 1.0 mW) pulses delivered to the pre-BötC during inspiration did not terminate activity, whereas stronger stimulations (= 2.0 mW) terminated inspiration. (2) When the pre-BötC stimulation ended in or was applied during expiration, rebound activation of inspiration occurred after a fixed latency. (3) Relatively weak sustained stimulation (20 Hz, 0.5–2.0 mW) of pre-BötC inhibitory neurons increased respiratory frequency, while a further increase of stimulus intensity (> 3.0 mW) reduced frequency and finally (= 5.0 mW) terminated respiratory oscillations. (4) Single pulses (0.2–5.0 s) applied to the BötC inhibited rhythmic activity for the duration of the stimulation. (5) Sustained stimulation (20 Hz, 0.5–3.0 mW) of the BötC reduced respiratory frequency and finally led to apnea. We have revised our computational model of pre-BötC and BötC microcircuits by incorporating an additional population of post-inspiratory inhibitory neurons in the pre-BötC that interacts with other neurons in the network. This model was able to reproduce the above experimental findings as well as previously published results of optogenetic activation of pre-BötC or BötC neurons obtained by other laboratories. The proposed organization of pre-BötC and BötC circuits leads to testable predictions about their specific roles in respiratory pattern generation and provides important insights into key circuit interactions operating within brainstem respiratory networks."
94. COREM: configurable retina simulator (Martínez-Cañada et al., 2016)
COREM is a configurable simulator for retina modeling that has been implemented within the framework of the Human Brain Project (HBP). The software platform can be interfaced with neural simulators (e.g., NEST) to connect with models of higher visual areas and with the Neurorobotics Platform of the HBP. The code is implemented in C++ and computations of spatiotemporal equations are optimized by means of recursive filtering techniques and multithreading. Most retina simulators are more focused on fitting specific retina functions. By contrast, the versatility of COREM allows the configuration of different retina models using a set of basic retina computational primitives. We implemented a series of retina models by combining these primitives to characterize some of the best-known phenomena observed in the retina: adaptation to the mean light intensity and temporal contrast, and differential motion sensitivity. The code has been extensively tested in Linux. The software can be also adapted to Mac OS. Installation instructions as well as the user manual can be found in the Github repository: https://github.com/pablomc88/COREM
95. Cortex-Basal Ganglia-Thalamus network model (Kumaravelu et al. 2016)
" ... We developed a biophysical network model comprising of the closed loop cortical-basal ganglia-thalamus circuit representing the healthy and parkinsonian rat brain. The network properties of the model were validated by comparing responses evoked in basal ganglia (BG) nuclei by cortical (CTX) stimulation to published experimental results. A key emergent property of the model was generation of low-frequency network oscillations. Consistent with their putative pathological role, low-frequency oscillations in model BG neurons were exaggerated in the parkinsonian state compared to the healthy condition. ..."
96. Cortical Basal Ganglia Network Model during Closed-loop DBS (Fleming et al 2020)
We developed a computational model of the cortical basal ganglia network to investigate closed-loop control of deep brain stimulation (DBS) for Parkinson’s disease (PD). The cortical basal ganglia network model incorporates the (i) the extracellular DBS electric field, (ii) antidromic and orthodromic activation of STN afferent fibers, (iii) the LFP detected at non-stimulating contacts on the DBS electrode and (iv) temporal variation of network beta-band activity within the thalamo-cortico-basal ganglia loop. The model facilitates investigation of clinically-viable closed-loop DBS control approaches, modulating either DBS amplitude or frequency, using an LFP derived measure of network beta-activity.
97. Cortical feedback alters visual response properties of dLGN relay cells (Martínez-Cañada et al 2018)
Network model that includes biophysically detailed, single-compartment and multicompartment neuron models of relay-cells and interneurons in the dLGN and a population of orientation-selective layer 6 simple cells, consisting of pyramidal cells (PY). We have considered two different arrangements of synaptic feedback from the ON and OFF zones in the visual cortex to the dLGN: phase-reversed (‘push-pull’) and phase-matched (‘push-push’), as well as different spatial extents of the corticothalamic projection pattern. This project is the result of a research work and its associated publication is: (Martínez-Cañada et al 2018). Installation instructions as well as the latest version can be found in the Github repository: https://github.com/CINPLA/biophysical_thalamocortical_system
98. Cortical model with reinforcement learning drives realistic virtual arm (Dura-Bernal et al 2015)
We developed a 3-layer sensorimotor cortical network of consisting of 704 spiking model-neurons, including excitatory, fast-spiking and low-threshold spiking interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a virtual musculoskeletal human arm, with realistic anatomical and biomechanical properties, to reach a target. Virtual arm position was used to simultaneously control a robot arm via a network interface.
99. Cortical oscillations and the basal ganglia (Fountas & Shanahan 2017)
"Although brain oscillations involving the basal ganglia (BG) have been the target of extensive research, the main focus lies disproportionally on oscillations generated within the BG circuit rather than other sources, such as cortical areas. We remedy this here by investigating the influence of various cortical frequency bands on the intrinsic effective connectivity of the BG, as well as the role of the latter in regulating cortical behaviour. To do this, we construct a detailed neural model of the complete BG circuit based on fine-tuned spiking neurons, with both electrical and chemical synapses as well as short-term plasticity between structures. As a measure of effective connectivity, we estimate information transfer between nuclei by means of transfer entropy. Our model successfully reproduces firing and oscillatory behaviour found in both the healthy and Parkinsonian BG. We found that, indeed, effective connectivity changes dramatically for different cortical frequency bands and phase offsets, which are able to modulate (or even block) information flow in the three major BG pathways. ..."
100. Current Dipole in Laminar Neocortex (Lee et al. 2013)
Laminar neocortical model in NEURON/Python, adapted from Jones et al 2009. https://bitbucket.org/jonescompneurolab/corticaldipole
101. Decoding movement trajectory from simulated grid cell population activity (Bush & Burgess 2019)
Matlab code to simulate a population of grid cells that exhibit both a rate and phase code for location in 1D or 2D environments, and are modulated by a human hippocampal LFP signal with highly variable frequency; then subsequently decode location, running speed, movement direction and an arbitrary fourth variable from population firing rates and phases in each oscillatory cycle.
102. Deconstruction of cortical evoked potentials generated by subthalamic DBS (Kumaravelu et al 2018)
"... High frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) suppresses parkinsonian motor symptoms and modulates cortical activity. ... Cortical evoked potentials (cEP) generated by STN DBS reflect the response of cortex to subcortical stimulation, and the goal was to determine the neural origin of cEP using a two-step approach. First, we recorded cEP over ipsilateral primary motor cortex during different frequencies of STN DBS in awake healthy and unilateral 6-OHDA lesioned parkinsonian rats. Second, we used a biophysically-based model of the thalamocortical network to deconstruct the neural origin of the cEP. The in vivo cEP included short (R1), intermediate (R2) and long-latency (R3) responses. Model-based cortical responses to simulated STN DBS matched remarkably well the in vivo responses. R1 was generated by antidromic activation of layer 5 pyramidal neurons, while recurrent activation of layer 5 pyramidal neurons via excitatory axon collaterals reproduced R2. R3 was generated by polysynaptic activation of layer 2/3 pyramidal neurons via the cortico-thalamic-cortical pathway. Antidromic activation of the hyperdirect pathway and subsequent intracortical and cortico-thalamo-cortical synaptic interactions were sufficient to generate cEP by STN DBS, and orthodromic activation through basal ganglia-thalamus-cortex pathways was not required. These results demonstrate the utility of cEP to determine the neural elements activated by STN DBS that might modulate cortical activity and contribute to the suppression of parkinsonian symptoms."
103. Default mode network model (Matsui et al 2014)
Default mode network (DMN) shows intrinsic, high-level activity at rest. We tested a hypothesis proposed for its role in sensory information processing: Intrinsic DMN activity facilitates neural responses to sensory input. A neural network model, consisting of a sensory network (Nsen) and a DMN, was simulated. The Nsen contained cell assemblies. Each cell assembly comprised principal cells, GABAergic interneurons (Ia, Ib), and glial cells. We let the Nsen carry out a perceptual task: detection of sensory stimuli. … This enabled the Nsen to reliably detect the stimulus. We suggest that intrinsic default model network activity may accelerate the reaction speed of the sensory network by modulating its ongoing-spontaneous activity in a subthreshold manner. Ambient GABA contributes to achieve an optimal ongoing spontaneous subthreshold neuronal state, in which GABAergic gliotransmission triggered by the intrinsic default model network activity may play an important role.
104. Dentate gyrus (Morgan et al. 2007, 2008, Santhakumar et al. 2005, Dyhrfjeld-Johnsen et al. 2007)
This model was implemented by Rob Morgan in the Soltesz lab at UC Irvine. It is a scaleable model of the rat dentate gyrus including four cell types. This model runs in serial (on a single processor) and has been published at the size of 50,000 granule cells (with proportional numbers of the other cells).
105. Dentate Gyrus Feed-forward inhibition (Ferrante et al. 2009)
In this paper, the model was used to show how that FFI can change a steeply sigmoidal input-output (I/O) curve into a double-sigmoid typical of buffer systems.
106. Dentate Gyrus model including Granule cells with dendritic compartments (Chavlis et al 2017)
Here we investigate the role of dentate granule cell dendrites in pattern separation. The model consists of point neurons (Integrate and fire) and in principal neurons, the granule cells, we have incorporated various number of dendrites.
107. Dentate gyrus network model (Santhakumar et al 2005)
Mossy cell loss and mossy fiber sprouting are two characteristic consequences of repeated seizures and head trauma. However, their precise contributions to the hyperexcitable state are not well understood. Because it is difficult, and frequently impossible, to independently examine using experimental techniques whether it is the loss of mossy cells or the sprouting of mossy fibers that leads to dentate hyperexcitability, we built a biophysically realistic and anatomically representative computational model of the dentate gyrus to examine this question. The 527-cell model, containing granule, mossy, basket, and hilar cells with axonal projections to the perforant-path termination zone, showed that even weak mossy fiber sprouting (10-15% of the strong sprouting observed in the pilocarpine model of epilepsy) resulted in the spread of seizure-like activity to the adjacent model hippocampal laminae after focal stimulation of the perforant path. See reference for more and details.
108. Dentate gyrus network model (Tejada et al 2014)
" ... Here we adapted an existing computational model of the dentate gyrus (J Neurophysiol 93: 437-453, 2005) by replacing the reduced granule cell models with morphologically detailed models coming from (3D) reconstructions of mature cells. ... Different fractions of the mature granule cell models were replaced by morphologically reconstructed models of newborn dentate granule cells from animals with PILO-induced Status Epilepticus, which have apical dendritic alterations and spine loss, and control animals, which do not have these alterations. This complex arrangement of cells and processes allowed us to study the combined effect of mossy fiber sprouting, altered apical dendritic tree and dendritic spine loss in newborn granule cells on the excitability of the dentate gyrus model. Our simulations suggest that alterations in the apical dendritic tree and dendritic spine loss in newborn granule cells have opposing effects on the excitability of the dentate gyrus after Status Epilepticus. Apical dendritic alterations potentiate the increase of excitability provoked by mossy fiber sprouting while spine loss curtails this increase. "
109. Dentate gyrus network model pattern separation and granule cell scaling in epilepsy (Yim et al 2015)
The dentate gyrus (DG) is thought to enable efficient hippocampal memory acquisition via pattern separation. With patterns defined as spatiotemporally distributed action potential sequences, the principal DG output neurons (granule cells, GCs), presumably sparsen and separate similar input patterns from the perforant path (PP). In electrophysiological experiments, we have demonstrated that during temporal lobe epilepsy (TLE), GCs downscale their excitability by transcriptional upregulation of ‘leak’ channels. Here we studied whether this cell type-specific intrinsic plasticity is in a position to homeostatically adjust DG network function. We modified an established conductance-based computer model of the DG network such that it realizes a spatiotemporal pattern separation task, and quantified its performance with and without the experimentally constrained leaky GC phenotype. ...
110. Development and Binocular Matching of Orientation Selectivity in Visual Cortex (Xu et al 2020)
This model investigates the development of orientation selectivity and its binocular matching in visual cortex by implementing a neuron that has plastic synapses for its inputs from the left and right eye. The plasticity is taken to be voltage-based with homeostasis (Clopath et al 2010). The neuron is modeled as an adaptive exponential integrate-fire neuron. The uploaded model has been used in Xu, Cang & Riecke (2020) to analyze the impact of ocular dominance and orientation selectivity on the matching process. There it has been found that the matching can proceed by a slow shifting or a sudden switching of the preferred orientation.
111. Development of orientation-selective simple cell receptive fields (Rishikesh and Venkatesh, 2003)
Implementation of a computational model for the development of simple-cell receptive fields spanning the regimes before and after eye-opening. The before eye-opening period is governed by a correlation-based rule from Miller (Miller, J. Neurosci., 1994), and the post eye-opening period is governed by a self-organizing, experience-dependent dynamics derived in the reference below.
112. Different roles for inhibition in the rhythm-generating respiratory network (Harris et al 2017)
"Unraveling the interplay of excitation and inhibition within rhythm-generating networks remains a fundamental issue in neuroscience. We use a biophysical model to investigate the different roles of local and long-range inhibition in the respiratory network, a key component of which is the pre-Bötzinger complex inspiratory microcircuit. ..."
113. Diffusive homeostasis in a spiking network model (Sweeney et al. 2015)
In this paper we propose a new mechanism, diffusive homeostasis, in which neural excitability is modulated by nitric oxide, a gas which can flow freely across cell membranes. Our model simulates the activity-dependent synthesis and diffusion of nitric oxide in a recurrent network model of integrate-and-fire neurons. The concentration of nitric oxide is then used as homeostatic readout which modulates the firing threshold of each neuron.
114. Disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex (Domanski et al 2019)
"Sensory hypersensitivity is a common and debilitating feature of neurodevelopmental disorders such as Fragile X Syndrome (FXS). How developmental changes in neuronal function culminate in network dysfunction that underlies sensory hypersensitivities is unknown. By systematically studying cellular and synaptic properties of layer 4 neurons combined with cellular and network simulations, we explored how the array of phenotypes in Fmr1-knockout (KO) mice produce circuit pathology during development. We show that many of the cellular and synaptic pathologies in Fmr1-KO mice are antagonistic, mitigating circuit dysfunction, and hence may be compensatory to the primary pathology. Overall, the layer 4 network in the Fmr1-KO exhibits significant alterations in spike output in response to thalamocortical input and distorted sensory encoding. This developmental loss of layer 4 sensory encoding precision would contribute to subsequent developmental alterations in layer 4-to-layer 2/3 connectivity and plasticity observed in Fmr1-KO mice, and circuit dysfunction underlying sensory hypersensitivity."
115. Distal inhibitory control of sensory-evoked excitation (Egger, Schmitt et al. 2015)
Model of a cortical layer (L) 2 pyramidal neuron embedded in an anatomically realistic network of two barrel columns in rat vibrissal cortex. This model is used to investigate the effects of spatially and temporally specific inhibition from L1 inhibitory interneurons on the sensory-evoked subthreshold responses of the L2 pyramidal neuron, and can be used to create simulation results underlying Figures 3D, 4B, 4C and 4E from (Egger, Schmitt et al. 2015).
116. Distance-dependent inhibition in the hippocampus (Strüber et al. 2017)
Network model of a hippocampal circuit including interneurons and principal cells. Amplitude and decay time course of inhibitory synapses can be systematically changed for different distances between connected cells. Various forms of excitatory drives can be administered to the network including spatially structured input.
117. Distributed cerebellar plasticity implements adaptable gain control (Garrido et al., 2013)
We tested the role of plasticity distributed over multiple synaptic sites (Hansel et al., 2001; Gao et al., 2012) by generating an analog cerebellar model embedded into a control loop connected to a robotic simulator. The robot used a three-joint arm and performed repetitive fast manipulations with different masses along an 8-shape trajectory. In accordance with biological evidence, the cerebellum model was endowed with both LTD and LTP at the PF-PC, MF-DCN and PC-DCN synapses. This resulted in a network scheme whose effectiveness was extended considerably compared to one including just PF-PC synaptic plasticity. Indeed, the system including distributed plasticity reliably self-adapted to manipulate different masses and to learn the arm-object dynamics over a time course that included fast learning and consolidation, along the lines of what has been observed in behavioral tests. In particular, PF-PC plasticity operated as a time correlator between the actual input state and the system error, while MF-DCN and PC-DCN plasticity played a key role in generating the gain controller. This model suggests that distributed synaptic plasticity allows generation of the complex learning properties of the cerebellum.
118. Distributed representation of perceptual categories in the auditory cortex (Kim and Bao 2008)
Examines the hypothesis that enlargement in cortical stimulus representation is a mechanism of categorical perception. Categorical perception is tested using discrimination and identification ability.
119. Distributed synaptic plasticity and spike timing (Garrido et al. 2013)
Here we have used a computational model to simulate the impact of multiple distributed synaptic weights in the cerebellar granular layer network. In response to mossy fiber bursts, synaptic weights at multiple connections played a crucial role to regulate spike number and positioning in granule cells. Interestingly, different combinations of synaptic weights optimized either first-spike timing precision or spike number, efficiently controlling transmission and filtering properties. These results predict that distributed synaptic plasticity regulates the emission of quasi-digital spike patterns on the millisecond time scale and allows the cerebellar granular layer to flexibly control burst transmission along the mossy fiber pathway.
120. Duration-tuned neurons from the inferior colliculus of the big brown bat (Aubie et al. 2009)
dtnet is a generalized neural network simulator written in C++ with an easy to use XML description language to generate arbitrary neural networks and then run simulations covering many different parameter values. For example, you can specify ranges of parameter values for several different connection weights and then automatically run simulations over all possible parameters. Graphing ability is built in as long as the free, open-source, graphing application GLE (http://glx.sourceforge.net/) is installed. Included in the examples folder are simulation descriptions that were used to generate the results in Aubie et al. (2009). Refer to the README file for instructions on compiling and running these examples. The most recent source code can be obtained from GitHub: <a href="https://github.com/baubie/dtnet">https://github.com/baubie/dtnet</a>
121. Duration-tuned neurons from the inferior colliculus of vertebrates (Aubie et al. 2012)
These models reproduce the responses of duration-tuned neurons in the auditory midbrain of the big brown bat, the rat, the mouse and the frog (Aubie et al. 2012). They are written in the Python interface to NEURON and a subset of the figures from Aubie et al. (2012) are pre-set in run.py (raw data is generated and a separate graphing program must be used to visualize the results).
122. Dynamic cortical interlaminar interactions (Carracedo et al. 2013)
"... Here we demonstrate the mechanism underlying a purely neocortical delta rhythm generator and show a remarkable laminar, cell subtype and local subcircuit delineation between delta and nested theta rhythms. We show that spike timing during delta-nested theta rhythms controls an iterative, reciprocal interaction between deep and superficial cortical layers resembling the unsupervised learning processes proposed for laminar neural networks by Hinton and colleagues ... and mimicking the alternating cortical dynamics of sensory and memory processing during wakefulness."
123. Dynamic dopamine modulation in the basal ganglia: Learning in Parkinson (Frank et al 2004,2005)
See README file for all info on how to run models under different tasks and simulated Parkinson's and medication conditions.
124. Dynamical patterns underlying response properties of cortical circuits (Keane et al 2018)
"Recent experimental studies show cortical circuit responses to external stimuli display varied dynamical properties. These include stimulus strength-dependent population response patterns, a shift from synchronous to asynchronous states and a decline in neural variability. To elucidate the mechanisms underlying these response properties and explore how they are mechanistically related, we develop a neural circuit model that incorporates two essential features widely observed in the cerebral cortex. The first feature is a balance between excitatory and inhibitory inputs to individual neurons; the second feature is distance-dependent connectivity. We show that applying a weak external stimulus to the model evokes a wave pattern propagating along lateral connections, but a strong external stimulus triggers a localized pattern; these stimulus strength-dependent population response patterns are quantitatively comparable with those measured in experimental studies. ..."
125. Dynamics in random NNs with multiple neuron subtypes (Pena et al 2018, Tomov et al 2014, 2016)
"Spontaneous cortical population activity exhibits a multitude of oscillatory patterns, which often display synchrony during slow-wave sleep or under certain anesthetics and stay asynchronous during quiet wakefulness. The mechanisms behind these cortical states and transitions among them are not completely understood. Here we study spontaneous population activity patterns in random networks of spiking neurons of mixed types modeled by Izhikevich equations. Neurons are coupled by conductance-based synapses subject to synaptic noise. We localize the population activity patterns on the parameter diagram spanned by the relative inhibitory synaptic strength and the magnitude of synaptic noise. In absence of noise, networks display transient activity patterns, either oscillatory or at constant level. The effect of noise is to turn transient patterns into persistent ones: for weak noise, all activity patterns are asynchronous non-oscillatory independently of synaptic strengths; for stronger noise, patterns have oscillatory and synchrony characteristics that depend on the relative inhibitory synaptic strength. ..."
126. Dynamics of sleep oscillations coupled to brain temperature on multiple scales (Csernai et al 2019)
"Every form of neural activity depends on temperature, yet its relationship to brain rhythms is poorly understood. In this work we examined how sleep spindles are influenced by changing brain temperatures and how brain temperature is influenced by sleep oscillations. We employed a novel thermoelectrode designed for measuring temperature while recording neural activity. We found that spindle frequency is positively correlated and duration negatively correlated with brain temperature. Local heating of the thalamus replicated the temperature dependence of spindle parameters in the heated area only, suggesting biophysical rather than global modulatory mechanisms, a finding also supported by a thalamic network model. Finally, we show that switches between oscillatory states also influence brain temperature on a shorter and smaller scale. Epochs of paradoxical sleep as well as the infra-slow oscillation were associated with brain temperature fluctuations below 0.2°C. Our results highlight that brain temperature is massively intertwined with sleep oscillations on various time scales."
127. Effect of polysynaptic facilitaiton between piriform-hippocampal network stages (Trieu et al 2015)
This is a model of a multistage network with stages representing regions and synaptic contacts from the olfactory cortex to region CA1 of the hippocampus in Brian2 spiking neural network simulator (Trieu et al 2015). It is primarily designed to assess how synaptic facilitation at multiple stages in response to theta firing changes the output of the network. Further developments will be posted at: github.com/cdcox/multistage_network This model was prepared by Conor D Cox, University of California, Irvine For questions please contact Conor at cdcox1@gmail.com
128. Effects of Guanfacine and Phenylephrine on a model of working memory (Duggins et al 2017)
"We use a spiking neural network model of working memory (WM) capable of performing the spatial delayed response task (DRT) to investigate two drugs that affect WM: guanfacine (GFC) and phenylephrine (PHE). In this model, the loss of information over time results from changes in the spiking neural activity through recurrent connections. We reproduce the standard forgetting curve and then show that this curve changes in the presence of GFC and PHE, whose application is simulated by manipulating functional, neural, and biophysical properties of the model. ... We compare our model to both electrophysiological data from neurons in monkey dorsolateral prefrontal cortex and to behavioral evidence from monkeys performing the DRT."
129. Effects of increasing CREB on storage and recall processes in a CA1 network (Bianchi et al. 2014)
Several recent results suggest that boosting the CREB pathway improves hippocampal-dependent memory in healthy rodents and restores this type of memory in an AD mouse model. However, not much is known about how CREB-dependent neuronal alterations in synaptic strength, excitability and LTP can boost memory formation in the complex architecture of a neuronal network. Using a model of a CA1 microcircuit, we investigate whether hippocampal CA1 pyramidal neuron properties altered by increasing CREB activity may contribute to improve memory storage and recall. With a set of patterns presented to a network, we find that the pattern recall quality under AD-like conditions is significantly better when boosting CREB function with respect to control. The results are robust and consistent upon increasing the synaptic damage expected by AD progression, supporting the idea that the use of CREB-based therapies could provide a new approach to treat AD.
130. Effects of spinal cord stimulation on WDR dorsal horn network (Zhang et al 2014)
" ... To study the mechanisms underlying SCS (Spinal cord stimulation), we constructed a biophysically-based network model of the dorsal horn circuit consisting of interconnected dorsal horn interneurons and a wide dynamic range (WDR) projection neuron and representations of both local and surround receptive field inhibition. We validated the network model by reproducing cellular and network responses relevant to pain processing including wind-up, A-fiber mediated inhibition, and surround receptive field inhibition. ..." See paper for more.
131. Efficient simulation environment for modeling large-scale cortical processing (Richert et al. 2011)
"We have developed a spiking neural network simulator, which is both easy to use and computationally efficient, for the generation of large-scale computational neuroscience models. The simulator implements current or conductance based Izhikevich neuron networks, having spike-timing dependent plasticity and short-term plasticity. ..."
132. Electrically-coupled Retzius neurons (Vazquez et al. 2009)
"Dendritic electrical coupling increases the number of effective synaptic inputs onto neurons by allowing the direct spread of synaptic potentials from one neuron to another. Here we studied the summation of excitatory postsynaptic potentials (EPSPs) produced locally and arriving from the coupled neuron (transjunctional) in pairs of electrically-coupled Retzius neurons of the leech. We combined paired recordings of EPSPs, the production of artificial EPSPs (APSPs) in neuron pairs with different coupling coefficients and simulations of EPSPs produced in the coupled dendrites. ..."
133. Electrodecrements in in vitro model of infantile spasms (Traub et al 2020)
The code is an extension of the thalamocortical model of Traub et al. (2005) J Neurophysiol. It is here applied to an in vitro model of the electrodecremental response seen in the EEG of children with infantile spasms (West syndrome)
134. Electrostimulation to reduce synaptic scaling driven progression of Alzheimers (Rowan et al. 2014)
"... As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. ... The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, ... Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. ... "
135. ELL pyramidal neuron (Simmonds and Chacron 2014)
network model of ELL pyramidal neurons receiving both feedforward and feedback inputs
136. Emergence of Connectivity Motifs in Networks of Model Neurons (Vasilaki, Giugliano 2014)
Recent evidence suggests that short-term dynamics of excitatory synaptic transmission is correlated to stereotypical connectivity motifs. We show that these connectivity motifs emerge in networks of model neurons, from the interactions between short-term synaptic dynamics (SD) and long-term spike-timing dependent plasticity (STDP).
137. Emergence of physiological oscillation frequencies in neocortex simulations (Neymotin et al. 2011)
"Coordination of neocortical oscillations has been hypothesized to underlie the "binding" essential to cognitive function. However, the mechanisms that generate neocortical oscillations in physiological frequency bands remain unknown. We hypothesized that interlaminar relations in neocortex would provide multiple intermediate loops that would play particular roles in generating oscillations, adding different dynamics to the network. We simulated networks from sensory neocortex using 9 columns of event-driven rule-based neurons wired according to anatomical data and driven with random white-noise synaptic inputs. ..."
138. Emergence of spatiotemporal sequences in spiking neuronal networks (Spreizer et al 2019)
"Spatio-temporal sequences of neuronal activity are observed in many brain regions in a variety of tasks and are thought to form the basis of meaningful behavior. However, mechanisms by which a neuronal network can generate spatio-temporal activity sequences have remained obscure. Existing models are biologically untenable because they either require manual embedding of a feedforward network within a random network or supervised learning to train the connectivity of a network to generate sequences. Here, we propose a biologically plausible, generative rule to create spatio-temporal activity sequences in a network of spiking neurons with distance-dependent connectivity. We show that the emergence of spatio- temporal activity sequences requires: (1) individual neurons preferentially project a small fraction of their axons in a specific direction, and (2) the preferential projection direction of neighboring neurons is similar. Thus, an anisotropic but correlated connectivity of neuron groups suffices to generate spatio-temporal activity sequences in an otherwise random neuronal network model."
139. Encoding and retrieval in a model of the hippocampal CA1 microcircuit (Cutsuridis et al. 2009)
This NEURON code implements a small network model (100 pyramidal cells and 4 types of inhibitory interneuron) of storage and recall of patterns in the CA1 region of the mammalian hippocampus. Patterns of PC activity are stored either by a predefined weight matrix generated by Hebbian learning, or by STDP at CA3 Schaffer collateral AMPA synapses.
140. Engaging distinct oscillatory neocortical circuits (Vierling-Claassen et al. 2010)
"Selective optogenetic drive of fast-spiking (FS) interneurons (INs) leads to enhanced local field potential (LFP) power across the traditional “gamma” frequency band (20–80 Hz; Cardin et al., 2009). In contrast, drive to regular-spiking (RS) pyramidal cells enhances power at lower frequencies, with a peak at 8 Hz. The first result is consistent with previous computational studies emphasizing the role of FS and the time constant of GABAA synaptic inhibition in gamma rhythmicity. However, the same theoretical models do not typically predict low-frequency LFP enhancement with RS drive. To develop hypotheses as to how the same network can support these contrasting behaviors, we constructed a biophysically principled network model of primary somatosensory neocortex containing FS, RS, and low-threshold spiking (LTS) INs. ..."
141. Epilepsy may be caused by very small functional changes in ion channels (Thomas et al. 2009)
We used a previously published model of the dentate gyrus with varying degrees of mossy fibre sprouting.We preformed a sensitivity analysis where we systematically varied individual properties of ion channels. The results predict that genetic variations in the properties of sodium channels are likely to have the biggest impact on network excitability. Furthermore, these changes may be as small as 1mV, which is currently undetectable using standard experimental practices.
142. Epileptic seizure model with Morris-Lecar neurons (Beverlin and Netoff 2011)
Here we use phase-response curves (PRC) from Morris-Lecar (M-L) model neurons with synaptic depression and gradually decrease input current to cells within a network simulation. This method effectively decreases firing rates resulting in a shift to greater network synchrony illustrating a possible mechanism of the transition phenomenon. PRCs are measured from the M-L conductance based model cell with a range of input currents within the limit cycle. A large network of 3000 excitatory neurons is simulated with a network topology generated from second-order statistics which allows a range of population synchrony. The population synchrony of the oscillating cells is measured with the Kuramoto order parameter, which reveals a transition from tonic to clonic phase exhibited by our model network.
143. Escape response latency in the Giant Fiber System of Drosophila melanogastor (Augustin et al 2019)
"The Giant Fiber System (GFS) is a multi-component neuronal pathway mediating rapid escape response in the adult fruit-fly Drosophila melanogaster, usually in the face of a threatening visual stimulus. Two branches of the circuit promote the response by stimulating an escape jump followed by flight initiation. Our recent work demonstrated an age-associated decline in the speed of signal propagation through the circuit, measured as the stimulus-to-muscle depolarization response latency. The decline is likely due to the diminishing number of inter-neuronal gap junctions in the GFS of ageing flies. In this work, we presented a realistic conductance-based, computational model of the GFS that recapitulates our experimental results and identifies some of the critical anatomical and physiological components governing the circuit's response latency. According to our model, anatomical properties of the GFS neurons have a stronger impact on the transmission than neuronal membrane conductance densities. The model provides testable predictions for the effect of experimental interventions on the circuit's performance in young and ageing flies."
144. Event-related simulation of neural processing in complex visual scenes (Mihalas et al. 2011)
"... We here present an environment for the implementation of large networks of generalized integrate-and-fire neurons which uses an asynchronous event-based algorithm. ... The neuronal network to be simulated and all parameters are defined in extendible markup language. A model of the primate early visual system is implemented. The use of the tool is illustrated by simulating the processing of both simple and complex visual scenes through retina, thalamus and primary visual cortex."
145. Excitatory and inhibitory interactions in populations of model neurons (Wilson and Cowan 1972)
Coupled nonlinear differential equations are derived for the dynamics of spatially localized populations containing both excitatory and inhibitory model neurons. Phase plane methods and numerical solutions are then used to investigate population responses to various types of stimuli. The results obtained show simple and multiple hysteresis phenomena and limit cycle activity. The latter is particularly interesting since the frequency of the limit cycle oscillation is found to be a monotonic function of stimulus intensity. Finally, it is proved that the existence of limit cycle dynamics in response to one class of stimuli implies the existence of multiple stable states and hysteresis in response to a different class of stimuli. The relation between these findings and a number of experiments is discussed.
146. Excitatory and inhibitory population activity (Bittner et al 2017) (Litwin-Kumar & Doiron 2017)
"Many studies use population analysis approaches, such as dimensionality reduction, to characterize the activity of large groups of neurons. To date, these methods have treated each neuron equally, without taking into account whether neurons are excitatory or inhibitory. We studied population activity structure as a function of neuron type by applying factor analysis to spontaneous activity from spiking networks with balanced excitation and inhibition. Throughout the study, we characterized population activity structure by measuring its dimensionality and the percentage of overall activity variance that is shared among neurons. First, by sampling only excitatory or only inhibitory neurons, we found that the activity structures of these two populations in balanced networks are measurably different. We also found that the population activity structure is dependent on the ratio of excitatory to inhibitory neurons sampled. Finally we classified neurons from extracellular recordings in the primary visual cortex of anesthetized macaques as putative excitatory or inhibitory using waveform classification, and found similarities with the neuron type-specific population activity structure of a balanced network with excitatory clustering. These results imply that knowledge of neuron type is important, and allows for stronger statistical tests, when interpreting population activity structure."
147. Excitotoxic loss of dopaminergic cells in PD (Muddapu et al 2019)
"... A couple of the proposed mechanisms, however, show potential for the development of a novel line of PD (Parkinson's disease) therapeutics. One of these mechanisms is the peculiar metabolic vulnerability of SNc (Substantia Nigra pars compacta) cells compared to other dopaminergic clusters; the other is the SubThalamic Nucleus (STN)-induced excitotoxicity in SNc. To investigate the latter hypothesis computationally, we developed a spiking neuron network-model of SNc-STN-GPe system. In the model, prolonged stimulation of SNc cells by an overactive STN leads to an increase in ‘stress’ variable; when the stress in a SNc neuron exceeds a stress threshold, the neuron dies. The model shows that the interaction between SNc and STN involves a positive-feedback due to which, an initial loss of SNc cells that crosses a threshold causes a runaway-effect, leading to an inexorable loss of SNc cells, strongly resembling the process of neurodegeneration. The model further suggests a link between the two aforementioned mechanisms of SNc cell loss. Our simulation results show that the excitotoxic cause of SNc cell loss might initiate by weak-excitotoxicity mediated by energy deficit, followed by strong-excitotoxicity, mediated by a disinhibited STN. A variety of conventional therapies were simulated to test their efficacy in slowing down SNc cell loss. Among them, glutamate inhibition, dopamine restoration, subthalamotomy and deep brain stimulation showed superior neuroprotective-effects in the proposed model."
148. Failure of Deep Brain Stimulation in a basal ganglia neuronal network model (Dovzhenok et al. 2013)
"… Recently, a lot of interest has been devoted to desynchronizing delayed feedback deep brain stimulation (DBS). ... This study explores the action of delayed feedback stimulation on partially synchronized oscillatory dynamics, similar to what one observes experimentally in parkinsonian patients. …" Implemented by Andrey Dovzhenok, to whom questions should be addressed.
149. Fast convergence of cerebellar learning (Luque et al. 2015)
The cerebellum is known to play a critical role in learning relevant patterns of activity for adaptive motor control, but the underlying network mechanisms are only partly understood. The classical long-term synaptic plasticity between parallel fibers (PFs) and Purkinje cells (PCs), which is driven by the inferior olive (IO), can only account for limited aspects of learning. Recently, the role of additional forms of plasticity in the granular layer, molecular layer and deep cerebellar nuclei (DCN) has been considered. In particular, learning at DCN synapses allows for generalization, but convergence to a stable state requires hundreds of repetitions. In this paper we have explored the putative role of the IO-DCN connection by endowing it with adaptable weights and exploring its implications in a closed-loop robotic manipulation task. Our results show that IO-DCN plasticity accelerates convergence of learning by up to two orders of magnitude without conflicting with the generalization properties conferred by DCN plasticity. Thus, this model suggests that multiple distributed learning mechanisms provide a key for explaining the complex properties of procedural learning and open up new experimental questions for synaptic plasticity in the cerebellar network.
150. Fast global oscillations in networks of I&F neurons with low firing rates (Brunel and Hakim 1999)
Dynamics of a network of sparsely connected inhibitory current-based integrate-and-fire neurons. Individual neurons fire irregularly at low rate but the network is in an oscillatory global activity regime where neurons are weakly synchronized.
151. Fast oscillations in inhibitory networks (Maex, De Schutter 2003)
We observed a new phenomenon of resonant synchronization in computer-simulated networks of inhibitory neurons in which the synaptic current has a delayed onset, reflecting finite spike propagation and synaptic transmission times. At the resonant level of network excitation, all neurons fire synchronously and rhythmically with a period approximately four times the mean delay of the onset of the inhibitory synaptic current. ... By varying the axonal delay of the inhibitory connections, networks with a realistic synaptic kinetics can be tuned to frequencies from 40 to >200 Hz. ... We conclude that the delay of the synaptic current is the primary parameter controlling the oscillation frequency of inhibitory networks and propose that delay-induced synchronization is a mechanism for fast brain rhythms that depend on intact inhibitory synaptic transmission.
152. Feedforward heteroassociative network with HH dynamics (Lytton 1998)
Using the original McCulloch-Pitts notion of simple on and off spike coding in lieu of rate coding, an Anderson-Kohonen artificial neural network (ANN) associative memory model was ported to a neuronal network with Hodgkin-Huxley dynamics.
153. First-Spike-Based Visual Categorization Using Reward-Modulated STDP (Mozafari et al. 2018)
"...Here, for the first time, we show that (Reinforcement Learning) RL can be used efficiently to train a spiking neural network (SNN) to perform object recognition in natural images without using an external classifier. We used a feedforward convolutional SNN and a temporal coding scheme where the most strongly activated neurons fire first, while less activated ones fire later, or not at all. In the highest layers, each neuron was assigned to an object category, and it was assumed that the stimulus category was the category of the first neuron to fire. ..."
154. Fixed point attractor (Hasselmo et al 1995)
"... In the model, cholinergic suppression of synaptic transmission at excitatory feedback synapses is shown to determine the extent to which activity depends upon new features of the afferent input versus components of previously stored representations. ..." See paper for more and details. The MATLAB script demonstrates the model of fixed point attractors mediated by excitatory feedback with subtractive inhibition in a continuous firing rate model.
155. Formation of synfire chains (Jun and Jin 2007)
"Temporally precise sequences of neuronal spikes that span hundreds of milliseconds are observed in many brain areas, including songbird premotor nucleus, cat visual cortex, and primary motor cortex. Synfire chains—networks in which groups of neurons are connected via excitatory synapses into a unidirectional chain—are thought to underlie the generation of such sequences. It is unknown, however, how synfire chains can form in local neural circuits, especially for long chains. Here, we show through computer simulation that long synfire chains can develop through spike-time dependent synaptic plasticity and axon remodeling—the pruning of prolific weak connections that follows the emergence of a finite number of strong connections. ..."
156. FRAT: An amygdala-centered model of fear conditioning (Krasne et al. 2011)
Model of Pavlovian fear conditioning and extinction (due to neuromodulator-controlled LTP on principal cells and inhibory interneurons)occur in amygdala and contextual representations are learned in hippocampus. Many properties of fear conditioning are accounted for.
157. Fronto-parietal visuospatial WM model with HH cells (Edin et al 2007)
1) J Cogn Neurosci: 3 structural mechanisms that had been hypothesized to underlie vsWM development during childhood were evaluated by simulating the model and comparing results to fMRI. It was concluded that inter-regional synaptic connection strength cause vsWM development. 2) J Integr Neurosci: Given the importance of fronto-parietal connections, we tested whether connection asymmetry affected resistance to distraction. We drew the conclusion that stronger frontal connections are beneficial. By comparing model results to EEG, we concluded that the brain indeed has stronger frontal-to-parietal connections than vice versa.
158. Fully-Asynchronous Cache-Efficient Simulation of Detailed Neural Networks (Magalhaes et al 2019)
"Modern asynchronous runtime systems allow the re-thinking of large-scale scientific applications. With the example of a simulator of morphologically detailed neural networks, we show how detaching from the commonly used bulk-synchronous parallel (BSP) execution allows for the increase of prefetching capabilities, better cache locality, and a overlap of computation and communication, consequently leading to a lower time to solution. Our strategy removes the operation of collective synchronization of ODEs’ coupling information, and takes advantage of the pairwise time dependency between equations, leading to a fully-asynchronous exhaustive yet not speculative stepping model. Combined with fully linear data structures, communication reduce at compute node level, and an earliest equation steps first scheduler, we perform an acceleration at the cache level that reduces communication and time to solution by maximizing the number of timesteps taken per neuron at each iteration. Our methods were implemented on the core kernel of the NEURON scientific application. Asynchronicity and distributed memory space are provided by the HPX runtime system for the ParalleX execution model. Benchmark results demonstrate a superlinear speed-up that leads to a reduced runtime compared to the bulk synchronous execution, yielding a speed-up between 25% to 65% across different compute architectures, and in the order of 15% to 40% for distributed executions."
159. Functional balanced networks with synaptic plasticity (Sadeh et al, 2015)
The model investigates the impact of learning on functional sensory networks. It uses large-scale recurrent networks of excitatory and inhibitory spiking neurons equipped with synaptic plasticity. It explains enhancement of orientation selectivity and emergence of feature-specific connectivity in visual cortex of rodents during development, as reported in experiments.
160. Functional consequences of cortical circuit abnormalities on gamma in schizophrenia (Spencer 2009)
"Schizophrenia is characterized by cortical circuit abnormalities, which might be reflected in gamma-frequency (30–100 Hz) oscillations in the electroencephalogram. Here we used a computational model of cortical circuitry to examine the effects that neural circuit abnormalities might have on gamma generation and network excitability. The model network consisted of 1000 leaky integrateand- fi re neurons with realistic connectivity patterns and proportions of neuron types [pyramidal cells (PCs), regular-spiking inhibitory interneurons, and fast-spiking interneurons (FSIs)]. ... The results of this study suggest that a multimodal approach, combining non-invasive neurophysiological and structural measures, might be able to distinguish between different neural circuit abnormalities in schizophrenia patients. ..."
161. Functional properties of dendritic gap junctions in Cerebellar Golgi cells (Szoboszlay et al. 2016)
" ... We investigated the properties of gap junctions in cerebellar interneurons by combining paired somato-somatic and somato-dendritic recordings, anatomical reconstructions, immunohistochemistry, electron microscopy, and modeling. By fitting detailed compartmental models of Golgi cells to their somato-dendritic voltage responses, we determined their passive electrical properties and the mean gap junction conductance (0.9 nS). ..."
162. Gamma and theta rythms in biophysical models of hippocampus circuits (Kopell et al. 2011)
" ... the main rhythms displayed by the hippocampus, the gamma (30–90 Hz) and theta (4–12 Hz) rhythms. We concentrate on modeling in vitro experiments, but with an eye toward possible in vivo implications. ... We use simpler biophysical models; all cells have a single compartment only, and the interneurons are restricted to two types: fast-spiking (FS) basket cells and oriens lacunosum-moleculare (O-LM) cells. ... , we aim not so much at reproducing dynamics in great detail, but at clarifying the essential mechanisms underlying the production of the rhythms and their interactions (Kopell, 2005). ..."
163. Gamma genesis in the basolateral amygdala (Feng et al 2019)
Using in vitro and in vivo data we develop the first large-scale biophysically and anatomically realistic model of the basolateral amygdala nucleus (BL), which reproduces the dynamics of the in vivo local field potential (LFP). Significantly, it predicts that BL intrinsically generates the transient gamma oscillations observed in vivo. The model permitted exploration of the poorly understood synaptic mechanisms underlying gamma genesis in BL, and the model's ability to compute LFPs at arbitrary numbers of recording sites provided insights into the characteristics of the spatial properties of gamma bursts. Furthermore, we show how gamma synchronizes principal cells to overcome their low firing rates while simultaneously promoting competition, potentially impacting their afferent selectivity and efferent drive, and thus emotional behavior.
164. Gamma oscillations in hippocampal interneuron networks (Bartos et al 2002)
To examine whether an interneuron network with fast inhibitory synapses can act as a gamma frequency oscillator, we developed an interneuron network model based on experimentally determined properties. In comparison to previous interneuron network models, our model was able to generate oscillatory activity with higher coherence over a broad range of frequencies (20-110 Hz). In this model, high coherence and flexibility in frequency control emerge from the combination of synaptic properties, network structure, and electrical coupling.
165. Gamma oscillations in hippocampal interneuron networks (Wang, Buzsaki 1996)
The authors investigated the hypothesis that 20-80Hz neuronal (gamma) oscillations can emerge in sparsely connected network models of GABAergic fast-spiking interneurons. They explore model NN synchronization and compare their results to anatomical and electrophysiological data from hippocampal fast spiking interneurons.
166. Gamma-beta alternation in the olfactory bulb (David, Fourcaud-Trocmé et al., 2015)
This model, a simplified olfactory bulb network with mitral and granule cells, proposes a framework for two regimes of oscillation in the olfactory bulb: 1 - a weak inhibition regime (with no granule spike) where the network oscillates in the gamma (40-90Hz) band 2 - a strong inhibition regime (with granule spikes) where the network oscillates in the beta (15-30Hz) band. Slow modulations of sensory and centrifugal inputs, phase shifted by a quarter of cycle, possibly combined with short term depression of the mitral to granule AMPA synapse, allows the network to alternate between the two regimes as observed in anesthetized animals.
167. Gap junction coupled network of striatal fast spiking interneurons (Hjorth et al. 2009)
Gap junctions between striatal FS neurons has very weak ability to synchronise spiking. Input uncorrelated between neighbouring neurons is shunted, while correlated input is not.
168. Gap junction plasticity as a mechanism to regulate network-wide oscillations (Pernelle et al 2018)
"Oscillations of neural activity emerge when many neurons repeatedly activate together and are observed in many brain regions, particularly during sleep and attention. Their functional role is still debated, but could be associated with normal cognitive processes such as memory formation or with pathologies such as schizophrenia and autism. Powerful oscillations are also a hallmark of epileptic seizures. Therefore, we wondered what mechanism could regulate oscillations. A type of neuronal coupling, called gap junctions, has been shown to promote synchronization between inhibitory neurons. Computational models show that when gap junctions are strong, neurons synchronize together. Moreover recent investigations show that the gap junction coupling strength is not static but plastic and dependent on the firing properties of the neurons. Thus, we developed a model of gap junction plasticity in a network of inhibitory and excitatory neurons. We show that gap junction plasticity can maintain the right amount of oscillations to prevent pathologies from emerging. Finally, we show that gap junction plasticity serves an additional functional role and allows for efficient and robust information transfer."
169. Gap-junction coupled network activity depends on coupled dendrites diameter (Gansert et al. 2007)
"... We have previously shown that the amplitude of electrical signals propagating across gap-junctionally coupled passive cables is maximized at a unique diameter. This suggests that threshold-dependent signals may propagate through gap junctions for a finite range of diameters around this optimal value. Here we examine the diameter dependence of action potential propagation across model networks of dendro-dendritically coupled neurons. The neurons in these models have passive soma and dendrites and an action potential-generating axon. We show that propagation of action potentials across gap junctions occurs only over a finite range of dendritic diameters and that propagation delay depends on this diameter. ...". See paper for more and details.
170. Gating of steering signals through phasic modulation of reticulospinal neurons (Kozlov et al. 2014)
" ... We use the lamprey as a model for investigating the role of this phasic modulation of the reticulospinal activity, because the brainstem–spinal cord networks are known down to the cellular level in this phylogenetically oldest extant vertebrate. We describe how the phasic modulation of reticulospinal activity from the spinal CPG ensures reliable steering/turning commands without the need for a very precise timing of on- or offset, by using a biophysically detailed large-scale (19,600 model neurons and 646,800 synapses) computational model of the lamprey brainstem–spinal cord network. To verify that the simulated neural network can control body movements, including turning, the spinal activity is fed to a mechanical model of lamprey swimming. ..."
171. Generating coherent patterns of activity from chaotic neural networks (Sussillo and Abbott 2009)
"Neural circuits display complex activity patterns both spontaneously and when responding to a stimulus or generating a motor output. How are these two forms of activity related? We develop a procedure called FORCE learning for modifying synaptic strengths either external to or within a model neural network to change chaotic spontaneous activity into a wide variety of desired activity patterns. ... Our results reproduce data on premovement activity in motor and premotor cortex, and suggest that synaptic plasticity may be a more rapid and powerful modulator of network activity than generally appreciated."
172. Generating oscillatory bursts from a network of regular spiking neurons (Shao et al. 2009)
Avian nucleus isthmi pars parvocellularis (Ipc) neurons are reciprocally connected with the tectal layer 10 (L10) neurons and respond with oscillatory bursts to visual stimulation. To elucidate mechanisms of oscillatory bursting in this network of regularly spiking neurons, we investigated an experimentally constrained model of coupled leaky integrate-and-fire neurons with spike-rate adaptation. The model reproduces the observed Ipc oscillatory bursting in response to simulated visual stimulation.
173. GLMCC validation neural network model (Kobayashi et al. 2019)
Network model of two populations of randomly connected inhibitory and excitatory neurons to validate method for reconstructing the neural circuitry developed in "Reconstructing Neuronal Circuitry from Parallel Spike Trains" by Ryota Kobayashi, Shuhei Kurita, Anno Kurth, Katsunori Kitano, Kenji Mizuseki, Markus Diesmann, Barry J. Richmond and Shigeru Shinomoto.
174. Graph-theoretical Derivation of Brain Structural Connectivity (Giacopelli et al 2020)
Brain connectivity at the single neuron level can provide fundamental insights into how information is integrated and propagated within and between brain regions. However, it is almost impossible to adequately study this problem experimentally and, despite intense efforts in the field, no mathematical description has been obtained so far. Here, we present a mathematical framework based on a graph-theoretical approach that, starting from experimental data obtained from a few small subsets of neurons, can quantitatively explain and predict the corresponding full network properties. This model also changes the paradigm with which large-scale model networks can be built, from using probabilistic/empiric connections or limited data, to a process that can algorithmically generate neuronal networks connected as in the real system.
175. Grid cell oscillatory interference with noisy network oscillators (Zilli and Hasselmo 2010)
To examine whether an oscillatory interference model of grid cell activity could work if the oscillators were noisy neurons, we implemented these simulations. Here the oscillators are networks (either synaptically- or gap-junction--coupled) of one or more noisy neurons (either Izhikevich's simple model or a Hodgkin-Huxley--type biophysical model) which drive a postsynaptic cell (which may be integrate-and-fire, resonate-and-fire, or the simple model) which should fire spatially as a grid cell if the simulation is successful.
176. Grid cell spatial firing models (Zilli 2012)
This package contains MATLAB implementations of most models (published from 2005 to 2011) of the hexagonal firing field arrangement of grid cells.
177. Grid cells from place cells (Castro & Aguiar, 2014)
" ...Here we present a novel model for the emergence of gridlike firing patterns that stands on two key hypotheses: (1) spatial information in GCs is provided from PC activity and (2) grid fields result from a combined synaptic plasticity mechanism involving inhibitory and excitatory neurons mediating the connections between PCs and GCs. ..."
178. Growth Rules for Repair of Asynch Irregular Networks after Peripheral Lesions (Sinha et al 2021)
A model of peripheral lesions and the resulting activity-dependent rewiring in a simplified balanced cortical network model that exhibits biologically realistic Asynchronous Irregular (AI) activity, used to derive activity dependent growth rules for different synaptic elements: dendritic and axonal.
179. H-currents effect on the fluctuation of gamma/beta oscillations (Avella-Gonzalez et al., 2015)
This model was designed to study the impact of H-currents on the dynamics of cortical oscillations, and in paticular on the occurrence of high and low amplitude episodes (HAE, LAE) in network oscillations. The H-current is a slow, hyperpolarization-activated, depolarizing current that contributes to neuronal resonance and membrane potential. We characterized amplitude fluctuations in network oscillations by measuring the average durations of HAEs and LAEs, and explored how these were modulated by trains of external spikes, both in the presence and absence of H-channels. We looked at HAE duration, the frequency and power of network oscillations, and the effect of H-channels on the temporal voltage profile in single cells. We found that H-currents increased the oscillation frequency and, in combination with external spikes, representing input from areas outside the network, strongly decreased the synchrony of firing. As a consequence, the oscillation power and the duration of episodes during which the network exhibited high-amplitude oscillations were greatly reduced in the presence of H-channels.
180. Half-center oscillator database of leech heart interneuron model (Doloc-Mihu & Calabrese 2011)
We have created a database (HCO-db) of instances of a half-center oscillator computational model [Hill et al., 2001] for analyzing how neuronal parameters influence network activity. We systematically explored the parameter space of about 10.4 million simulated HCO instances and corresponding isolated neuron model simulations obtained by varying a set of selected parameters (maximal conductance of intrinsic and synaptic currents) in all combinations using a brute-force approach. We classified these HCO instances by their activity characteristics into identifiable groups. We built an efficient relational database table (HCO-db) with the resulting instances characteristics.
181. Hierarchical network model of perceptual decision making (Wimmer et al 2015)
Neuronal variability in sensory cortex predicts perceptual decisions. To investigate the interaction of bottom-up and top-down mechanisms during the decision process, we developed a hierarchical network model. The network consists of two circuits composed of leaky integrate-and-fire neurons: an integration circuit (e.g. LIP, FEF) and a sensory circuit (MT), recurrently coupled via bottom-up feedforward connections and top-down feedback connections. The integration circuit accumulates sensory evidence and produces a binary categorization due to winner-take-all competition between two decision-encoding populations (X.J. Wang, Neuron, 2002). The sensory circuit is a balanced randomly connected EI-network, that contains neural populations selective to opposite directions of motion. We have used this model to simulate a standard two-alternative forced-choice motion discrimination task.
182. High dimensional dynamics and low dimensional readouts in neural microcircuits (Haeusler et al 2006)
We investigate generic models for cortical microcircuits, i.e. recurrent circuits of integrate-and fire neurons with dynamic synapses. These complex dynamic systems subserve the amazing information processing capabilities of the cortex, but are at the present time very little understood. We analyze the transient dynamics of models for neural microcircuits from the point of view of one or two readout neurons that collapse the high dimensional transient dynamics of a neural circuit into a 1- or 2--dimensional output stream. See paper for more and details.
183. High frequency oscillations in a hippocampal computational model (Stacey et al. 2009)
"... Using a physiological computer model of hippocampus, we investigate random synaptic activity (noise) as a potential initiator of HFOs (high-frequency oscillations). We explore parameters necessary to produce these oscillations and quantify the response using the tools of stochastic resonance (SR) and coherence resonance (CR). ... Our results show that, under normal coupling conditions, synaptic noise was able to produce gamma (30–100 Hz) frequency oscillations. Synaptic noise generated HFOs in the ripple range (100–200 Hz) when the network had parameters similar to pathological findings in epilepsy: increased gap junctions or recurrent synaptic connections, loss of inhibitory interneurons such as basket cells, and increased synaptic noise. ... We propose that increased synaptic noise and physiological coupling mechanisms are sufficient to generate gamma oscillations and that pathologic changes in noise and coupling similar to those in epilepsy can produce abnormal ripples."
184. High frequency stimulation of the Subthalamic Nucleus (Rubin and Terman 2004)
" ... Using a computational model, this paper considers the hypothesis that DBS works by replacing pathologically rhythmic basal ganglia output with tonic, high frequency firing. In our simulations of parkinsonian conditions, rhythmic inhibition from GPi to the thalamus compromises the ability of thalamocortical relay (TC) cells to respond to depolarizing inputs, such as sensorimotor signals. High frequency stimulation of STN regularizes GPi firing, and this restores TC responsiveness, despite the increased frequency and amplitude of GPi inhibition to thalamus that result. We provide a mathematical phase plane analysis of the mechanisms that determine TC relay capabilities in normal, parkinsonian, and DBS states in a reduced model. This analysis highlights the differences in deinactivation of the low-threshold calcium T -current that we observe in TC cells in these different conditions. ..."
185. Hippocampal basket cell gap junction network dynamics (Saraga et al. 2006)
2 cell network of hippocampal basket cells connected by gap junctions. Paper explores how distal gap junctions and active dendrites can tune network dynamics.
186. Hippocampal CA1 NN with spontaneous theta, gamma: full scale & network clamp (Bezaire et al 2016)
This model is a full-scale, biologically constrained rodent hippocampal CA1 network model that includes 9 cells types (pyramidal cells and 8 interneurons) with realistic proportions of each and realistic connectivity between the cells. In addition, the model receives realistic numbers of afferents from artificial cells representing hippocampal CA3 and entorhinal cortical layer III. The model is fully scaleable and parallelized so that it can be run at small scale on a personal computer or large scale on a supercomputer. The model network exhibits spontaneous theta and gamma rhythms without any rhythmic input. The model network can be perturbed in a variety of ways to better study the mechanisms of CA1 network dynamics. Also see online code at http://bitbucket.org/mbezaire/ca1 and further information at http://mariannebezaire.com/models/ca1
187. Hippocampal CA3 network and circadian regulation (Stanley et al. 2013)
This model produces the hippocampal CA3 neural network model used in the paper below. It has two modes of operation, a default mode and a circadian mode. In the circadian mode, parameters are swept through a range of values. This model can be quite easily adapted to produce theta and gamma oscillations, as certain parameter sweeps will reveal (see Figures). BASH scripts interact with GENESIS 2.3 to implement parameter sweeps. The model contains four cell types derived from prior papers. CA3 pyramidal are derived from Traub et al (1991); Basket, stratum oriens (O-LM), and Medial Septal GABAergic (MSG) interneurons are taken from Hajos et al (2004).
188. Hippocampal spiking model for context dependent behavior (Raudies & Hasselmo 2014)
Our model simulates the effect of context dependent behavior using discrete inputs to drive spiking activity representing place and item followed sequentially by a discrete representation of the motor actions involving a response to an item (digging for food) or the movement to a different item (movement to a different pot for food). This simple network was able to consistently learn the context-dependent responses.
189. Hippocampus temporo-septal engram shift model (Lytton 1999)
Temporo-septal engram shift model of hippocampal memory. The model posits that memories gradually move along the hippocampus from a temporal encoding site to ever more septal sites from which they are recalled. We propose that the sense of time is encoded by the location of the engram along the temporo-septal axis.
190. Homeostatic mechanisms may shape oscillatory modulations (Peterson & Voytek 2020)
"Neural oscillations are observed ubiquitously in the mammalian brain, but their stability is known to be rather variable. Some oscillations are tonic and last for seconds or even minutes. Other oscillations appear as unstable bursts. Likewise, some oscillations rely on excitatory AMPAergic synapses, but others are GABAergic and inhibitory. Why this diversity exists is not clear. We hypothesized Ca2+-dependent homeostasis could be important in finding an explanation. We tested this hypothesis in a highly simplified model of hippocampal neurons. In this model homeostasis profoundly alters the modulatory effect of neural oscillations. Under homeostasis, tonic AMPAergic oscillations actually decrease excitability and desynchronize firing. Tonic oscillations that are synaptically GABAergic-like those in real hippocampus-don't provoke a homeostatic response, however. If our simple model is correct, homeostasis can explain why the theta rhythm in the hippocampus is synaptically inhibitory: GABA has little to no intrinsic homeostatic response, and so can preserve the pyramidal cell's natural dynamic range. Based on these results we can also speculate that homeostasis may explain why AMPAergic oscillations in cortex, and hippocampus, often appear as bursts. Bursts do not interact with the slow homeostatic time constant, and so retain their normal excitatory effect."
191. Homosynaptic plasticity in the tail withdrawal circuit (TWC) of Aplysia (Baxter and Byrne 2006)
The tail-withdrawal circuit of Aplysia provides a useful model system for investigating synaptic dynamics. Sensory neurons within the circuit manifest several forms of synaptic plasticity. Here, we developed a model of the circuit and investigated the ways in which depression (DEP) and potentiation (POT) contributed to information processing. DEP limited the amount of motor neuron activity that could be elicited by the monosynaptic pathway alone. POT within the monosynaptic pathway did not compensate for DEP. There was, however, a synergistic interaction between POT and the polysynaptic pathway. This synergism extended the dynamic range of the network, and the interplay between DEP and POT made the circuit respond preferentially to long-duration, low-frequency inputs.
192. Hopfield and Brody model (Hopfield, Brody 2000)
NEURON implementation of the Hopfield and Brody model from the papers: JJ Hopfield and CD Brody (2000) JJ Hopfield and CD Brody (2001). Instructions are provided in the below readme.txt file.
193. Hopfield and Brody model (Hopfield, Brody 2000) (NEURON+python)
Demonstration of Hopfield-Brody snychronization using artificial cells in NEURON+python.
194. Human Attentional Networks: A Connectionist Model (Wang and Fan 2007)
"... We describe a connectionist model of human attentional networks to explore the possible interplays among the networks from a computational perspective. This model is developed in the framework of leabra (local, error-driven, and associative, biologically realistic algorithm) and simultaneously involves these attentional networks connected in a biologically inspired way. ... We evaluate the model by simulating the empirical data collected on normal human subjects using the Attentional Network Test (ANT). The simulation results fit the experimental data well. In addition, we show that the same model, with a single parameter change that affects executive control, is able to simulate the empirical data collected from patients with schizophrenia. This model represents a plausible connectionist explanation for the functional structure and interaction of human attentional networks."
195. Human sleep/wake cycle (Rempe et al. 2010)
This model simulates sleep in the human brain and is consistent with both the flip/flop concept and the two-process model of sleep regulation. The model also gives a possible mechanism for the changes in sleep timing seen in narcolepsy.
196. Human tactile FA1 neurons (Hay and Pruszynski 2020)
"... we show that synaptic integration across the complex signals from the first-order neuronal population could underlie human ability to accurately (< 3°) and rapidly process the orientation of edges moving across the fingertip. We first derive spiking models of human first-order tactile neurons that fit and predict responses to moving edges with high accuracy. We then use the model neurons in simulating the peripheral neuronal population that innervates a fingertip. We train classifiers performing synaptic integration across the neuronal population activity, and show that synaptic integration across first-order neurons can process edge orientations with high acuity and speed. ... our models suggest that integration of fast-decaying (AMPA-like) synaptic inputs within short timescales is critical for discriminating fine orientations, whereas integration of slow-decaying (NMDA-like) synaptic inputs supports discrimination of coarser orientations and maintains robustness over longer timescales"
197. Huntington`s disease model (Gambazzi et al. 2010)
"Although previous studies of Huntington’s disease (HD) have addressed many potential mechanisms of striatal neuron dysfunction and death, it is also known based on clinical findings that cortical function is dramatically disrupted in HD. With respect to disease etiology, however, the specific molecular and neuronal circuit bases for the cortical effects of mutant huntingtin (htt) have remained largely unknown. In the present work we studied the relation between the molecular effects of mutant htt fragments in cortical cells and the corresponding behavior of cortical neuron microcircuits using a novel cellular model of HD. We observed that a transcript-selective diminution in activity-dependent BDNF expression preceded the onset of a synaptic connectivity deficit in ex vivo cortical networks, which manifested as decreased spontaneous collective burst-firing behavior measured by multi-electrode array substrates. Decreased BDNF expression was determined to be a significant contributor to network-level dysfunction, as shown by the ability of exogenous BDNF to ameliorate cortical microcircuit burst firing. The molecular determinants of the dysregulation of activity-dependent BDNF expression by mutant htt appear to be distinct from previously elucidated mechanisms, as they do not involve known NRSF/REST-regulated promoter sequences, but instead result from dysregulation of BDNF exon IV and VI transcription. These data elucidate a novel HD-related deficit in BDNF gene regulation as a plausible mechanism of cortical neuron hypoconnectivity and cortical function deficits in HD. Moreover, the novel model paradigm established here is well-suited to further mechanistic and drug screening research applications. A simple mathematical model is proposed to interpret the observations and to explore the impact of specific synaptic dysfunctions on network activity. Interestingly, the model predicts a decrease in synaptic connectivity to be an early effect of mutant huntingtin in cortical neurons, supporting the hypothesis of decreased, rather than increased, synchronized cortical firing in HD."
198. Hybrid oscillatory interference / continuous attractor NN of grid cell firing (Bush & Burgess 2014)
Matlab code to simulate a hybrid oscillatory interference - continuous attractor network model of grid cell firing in pyramidal and stellate cells of rodent medial entorhinal cortex
199. Hyperconnectivity, slow synapses in PFC mental retardation and autism model (Testa-Silva et al 2011)
The subdirectory 'matlab' contains MATLAB scripts (The Mathworks, USA) that can be used to reproduce the panels of Figures 4-5. This directory contains files to reproduce sample computer simulations presented in the 2011 paper authored by Meredith, R., Testa-Silva, G., Loebel, A., Giugliano, M., de Kock, C.; Mansvelder, H. "Hyperconnectivity and slow synapses in prefrontal cortex of a model for mental retardation and autism". ABSTRACT "... We propose that these findings are tightly linked: using a network model, we show that slower synapses are essential to counterbalance hyperconnectivity in order to maintain a dynamic range of excitatory activity. However, the slow synaptic time constants induce decreased responsiveness to low frequency stimulation, which may explain deficits in integration and information processing in attentional neuronal networks in neurodevelopmental disorders."
200. I&F recurrent networks with current- or conductance-based synapses (Cavallari et al. 2014)
Recurrent networks of two populations (excitatory and inhibitory) of randomly connected Leaky Integrate-and-Fire (LIF) neurons with either current- or conductance-based synapses from the paper S. Cavallari, S. Panzeri and A. Mazzoni (2014)
201. Ih tunes oscillations in an In Silico CA3 model (Neymotin et al. 2013)
" ... We investigated oscillatory control using a multiscale computer model of hippocampal CA3, where each cell class (pyramidal, basket, and oriens-lacunosum moleculare cells), contained type-appropriate isoforms of Ih. Our model demonstrated that modulation of pyramidal and basket Ih allows tuning theta and gamma oscillation frequency and amplitude. Pyramidal Ih also controlled cross-frequency coupling (CFC) and allowed shifting gamma generation towards particular phases of the theta cycle, effected via Ih’s ability to set pyramidal excitability. ..."
202. In silico hippocampal modeling for multi-target pharmacotherapy in schizophrenia (Sherif et al 2020)
"Using a hippocampal CA3 computer model with 1200 neurons, we examined the effects of alterations in NMDAR, HCN (Ih current), and GABAAR on information flow (measured with normalized transfer entropy), and in gamma activity in local field potential (LFP). We found that altering NMDARs, GABAAR, Ih, individually or in combination, modified information flow in an inverted-U shape manner, with information flow reduced at low and high levels of these parameters. Theta-gamma phase-amplitude coupling also had an inverted-U shape relationship with NMDAR augmentation. The strong information flow was associated with an intermediate level of synchrony, seen as an intermediate level of gamma activity in the LFP, and an intermediate level of pyramidal cell excitability"
203. Inferior Olive, subthreshold oscillations (Torben-Nielsen, Segev, Yarom 2012)
The Inferior Olive is a brain structure in which neurons are solely connected to each other through gap-junctions. Its behavior is characterized by spontaneous subthreshold oscillation, frequency changes in the subthreshold oscillation, stable phase differences between neurons, and propagating waves of activity. Our model based on actual IO topology can reproduce these behaviors and provides a mechanistic explanation thereof.
204. Information-processing in lamina-specific cortical microcircuits (Haeusler and Maass 2006)
A major challenge for computational neuroscience is to understand the computational function of lamina-specific synaptic connection patterns in stereotypical cortical microcircuits.We approach this problem by studying ... the dynamical system defined by more realistic cortical microcircuit models as a whole and by investigating the influence that its laminar structure has on the transmission and fusion of information within this dynamical system. The circuit models that we examine consist of Hodgkin--Huxley neurons with dynamic synapses... We investigate to what extent this cortical microcircuit template supports the accumulation and fusion of information contained in generic spike inputs into layer 4 and layers 2/3 and how well it makes this information accessible to projection neurons in layers 2/3 and layer 5. ... We conclude that computer simulations of detailed lamina-specific cortical microcircuit models provide new insight into computational consequences of anatomical and physiological data. See paper for more and details.
205. Inhibition and glial-K+ interaction leads to diverse seizure transition modes (Ho & Truccolo 2016)
"How focal seizures initiate and evolve in human neocortex remains a fundamental problem in neuroscience. Here, we use biophysical neuronal network models of neocortical patches to study how the interaction between inhibition and extracellular potassium ([K+]o) dynamics may contribute to different types of focal seizures. Three main types of propagated focal seizures observed in recent intracortical microelectrode recordings in humans were modelled ..."
206. Inhibition perturbations reveals dynamical structure of neural processing (Sadeh & Clopath 2020)
"Perturbation of neuronal activity is key to understanding the brain's functional properties, however, intervention studies typically perturb neurons in a nonspecific manner. Recent optogenetics techniques have enabled patterned perturbations, in which specific patterns of activity can be invoked in identified target neurons to reveal more specific cortical function. Here, we argue that patterned perturbation of neurons is in fact necessary to reveal the specific dynamics of inhibitory stabilization, emerging in cortical networks with strong excitatory and inhibitory functional subnetworks, as recently reported in mouse visual cortex. We propose a specific perturbative signature of these networks and investigate how this can be measured under different experimental conditions. Functionally, rapid spontaneous transitions between selective ensembles of neurons emerge in such networks, consistent with experimental results. Our study outlines the dynamical and functional properties of feature-specific inhibitory-stabilized networks, and suggests experimental protocols that can be used to detect them in the intact cortex."
207. Inhibitory cells enable sparse coding in V1 model (King et al. 2013)
" ... Here we show that adding a separate population of inhibitory neurons to a spiking model of V1 provides conformance to Dale’s Law, proposes a computational role for at least one class of interneurons, and accounts for certain observed physiological properties in V1. ... "
208. Inhibitory control by an integral feedback signal in prefrontal cortex (Miller and Wang 2006)
The prefrontal cortex (PFC) is known to be critical for inhibitory control of behavior, but the underlying mechanisms are unclear. Here, we propose that inhibitory control can be instantiated by an integral signal derived from working memory, another key function of the PFC. Speci&#64257;cally, we assume that an integrator converts excitatory input into a graded mnemonic activity that provides an inhibitory signal (integral feedback control) to upstream afferent neurons. We demonstrate this scenario in a neuronal-network model for a temporal discrimination task... See paper for details and more.
209. Inhibitory neuron plasticity as a mechanism for ocular dominance plasticity (Bono & Clopath 2019)
"Ocular dominance plasticity is a well-documented phenomenon allowing us to study properties of cortical maturation. Understanding this maturation might be an important step towards unravelling how cortical circuits function. However, it is still not fully understood which mechanisms are responsible for the opening and closing of the critical period for ocular dominance and how changes in cortical responsiveness arise after visual deprivation. In this article, we present a theory of ocular dominance plasticity. Following recent experimental work, we propose a framework where a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult animals. In this framework, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibition as well as excitatory-to-inhibitory synaptic plasticity. In our model, the former is responsible for the opening of the critical period, while the latter limits the plasticity in adult animals. Finally, we also provide a possible explanation for the variability in ocular dominance shifts observed in individual neurons and for the counter-intuitive shifts towards the closed eye."
210. Interaction of leak and IMI conductance on the STG over broad temperature range (Stadele et al 2015)
The ZIP file contains a Hodgkin-Huxley based circuit model and the simulation environment MadSim used to study the interaction of leak and IMI on the gastric mill network of the crab (Cancer borealis) as represented in (C. Städele, S. Heigele and W. Stein, 2015) MadSim, the simulation environment used for this study, is freeware and included in the package.
211. Interaural time difference detection by slowly integrating neurons (Vasilkov Tikidji-Hamburyan 2012)
For localization of a sound source, animals and humans process the microsecond interaural time differences of arriving sound waves. How nervous systems, consisting of elements with time constants of about and more than 1 ms, can reach such high precision is still an open question. This model shows that population of 10000 slowly integrating Hodgkin-Huxley neurons with inhibitory and excitatory inputs (EI neurons) can detect minute temporal disparities in input signals which are significantly less than any time constant in the system.
212. Investigation of different targets in deep brain stimulation for Parkinson`s (Pirini et al. 2009)
"We investigated by a computational model of the basal ganglia the different network effects of deep brain stimulation (DBS) for Parkinson’s disease (PD) in different target sites in the subthalamic nucleus (STN), the globus pallidus pars interna (GPi), and the globus pallidus pars externa (GPe). A cellular-based model of the basal ganglia system (BGS), based on the model proposed by Rubin and Terman (J Comput Neurosci 16:211–235, 2004), was developed. ... Our results suggest that DBS in the STN could functionally restore the TC relay activity, while DBS in the GPe and in the GPi could functionally over-activate and inhibit it, respectively. Our results are consistent with the experimental and the clinical evidences on the network effects of DBS."
213. Irregular spiking in NMDA-driven prefrontal cortex neurons (Durstewitz and Gabriel 2006)
Slow N-Methyl-D-aspartic acid (NMDA) synaptic currents are assumed to strongly contribute to the persistently elevated firing rates observed in prefrontal cortex (PFC) during working memory. During persistent activity, spiking of many neurons is highly irregular. ... The highest interspike-interval (ISI) variability occurred in a transition regime where the subthreshold membrane potential distribution shifts from mono- to bimodality, ... Predictability within irregular ISI series was significantly higher than expected from a noise-driven linear process, indicating that it might best be described through complex (potentially chaotic) nonlinear deterministic processes. Accordingly, the phenomena observed in vitro could be reproduced in purely deterministic biophysical model neurons. High spiking irregularity in these models emerged within a chaotic, close-to-bifurcation regime characterized by a shift of the membrane potential distribution from mono- to bimodality and by similar ISI return maps as observed in vitro. ... NMDA-induced irregular dynamics may have important implications for computational processes during working memory and neural coding.
214. JitCon: Just in time connectivity for large spiking networks (Lytton et al. 2008)
This simulation is primarily an illustration and is not well optimized for actually running large networks. jitcon.mod contains a large amount of C level code, understanding of which requires some knowledge of Neuron internals
215. Ketamine disrupts theta modulation of gamma in a computer model of hippocampus (Neymotin et al 2011)
"Abnormalities in oscillations have been suggested to play a role in schizophrenia. We studied theta-modulated gamma oscillations in a computer model of hippocampal CA3 in vivo with and without simulated application of ketamine, an NMDA receptor antagonist and psychotomimetic. Networks of 1200 multi-compartment neurons (pyramidal, basket and oriens-lacunosum moleculare, OLM, cells) generated theta and gamma oscillations from intrinsic network dynamics: basket cells primarily generated gamma and amplified theta, while OLM cells strongly contributed to theta. ..."
216. KInNeSS : a modular framework for computational neuroscience (Versace et al. 2008)
The xml files provided here implement a network of excitatory and inhibitory spiking neurons, governed by either Hodgkin-Huxley or quadratic integrate-and-fire dynamical equations. The code is used to demonstrate the capabilities of the KInNeSS software package for simulation of networks of spiking neurons. The simulation protocol used here is meant to facilitate the comparison of KInNeSS with other simulators reviewed in <a href="http://dx.doi.org/10.1007/s10827-007-0038-6">Brette et al. (2007)</a>. See the associated paper "Versace et al. (2008) KInNeSS : a modular framework for computational neuroscience." for an extensive description of KInNeSS .
217. Knox implementation of Destexhe 1998 spike and wave oscillation model (Knox et al 2018)
" ...The aim of this study was to use an established thalamocortical computer model to determine how T-type calcium channels work in concert with cortical excitability to contribute to pathogenesis and treatment response in CAE. METHODS: The model is comprised of cortical pyramidal, cortical inhibitory, thalamocortical relay, and thalamic reticular single-compartment neurons, implemented with Hodgkin-Huxley model ion channels and connected by AMPA, GABAA , and GABAB synapses. Network behavior was simulated for different combinations of T-type calcium channel conductance, inactivation time, steady state activation/inactivation shift, and cortical GABAA conductance. RESULTS: Decreasing cortical GABAA conductance and increasing T-type calcium channel conductance converted spindle to spike and wave oscillations; smaller changes were required if both were changed in concert. In contrast, left shift of steady state voltage activation/inactivation did not lead to spike and wave oscillations, whereas right shift reduced network propensity for oscillations of any type...."
218. L4 cortical barrel NN model receiving thalamic input during whisking or touch (Gutnisky et al. 2017)
Excitatory neurons in layer 4 (L4) in the barrel cortex respond relatively strongly to touch but not to whisker movement (Yu et al., Nat. Neurosci. 2016). The model explains the mechanism underlying this effect. The network is settled to filter out most stationary inputs. Brief touch input passes through because it takes time until feed-forward inhibition silences excitatory neurons receiving brief and strong thalamic excitation.
219. Laminar analysis of excitatory circuits in vibrissal motor and sensory cortex (Hooks et al. 2011)
"... We mapped local excitatory pathways in each area (primary motor cortex (vM1), primary somatosensory cortex (vS1; barrel cortex), and secondary somatosensory cortex (S2)) across all cortical layers using glutamate uncaging and laser scanning photostimulation. We analyzed these maps to derive laminar connectivity matrices describing the average strengths of pathways between individual neurons in different layers and between entire cortical layers. ..."
220. Laminar connectivity matrix simulation (Weiler et al 2008)
A routine that simulates the flow of activity within and across laminar levels in the local pyramidal neuron network, based on a connectivity matrix (W) measured by laser scanning photostimulation in mouse somatic motor cortex, and a very simple neural network simulation.
221. Large cortex model with map-based neurons (Rulkov et al 2004)
We develop a new computationally efficient approach for the analysis of complex large-scale neurobiological networks. Its key element is the use of a new phenomenological model of a neuron capable of replicating important spike pattern characteristics and designed in the form of a system of difference equations (a map). ... Interconnected with synaptic currents these model neurons demonstrated responses very similar to those found with Hodgkin-Huxley models and in experiments. We illustrate the efficacy of this approach in simulations of one- and two-dimensional cortical network models consisting of regular spiking neurons and fast spiking interneurons to model sleep and activated states of the thalamocortical system. See paper for more.
222. Large scale model of the olfactory bulb (Yu et al., 2013)
The readme file currently contains links to the results for all the 72 odors investigated in the paper, and the movie showing the network activity during learning of odor k3-3 (an aliphatic ketone).
223. Large scale neocortical model for PGENESIS (Crone et al 2019)
This is model code for a large scale neocortical model based on Traub et al. (2005), modified to run on PGENESIS on supercomputing resources. "In this paper (Crone et al 2019), we evaluate the computational performance of the GEneral NEural SImulation System (GENESIS) for large scale simulations of neural networks. While many benchmark studies have been performed for large scale simulations with leaky integrate-and-fire neurons or neuronal models with only a few compartments, this work focuses on higher fidelity neuronal models represented by 50–74 compartments per neuron. ..."
224. Large-scale model of neocortical slice in vitro exhibiting persistent gamma (Tomsett et al. 2014)
This model contains 15 neuron populations (8 excitatory, 7 inhibitory) arranged into 4 cortical layers (layer 1 empty, layers 2/3 combined). It produces a persistent gamma oscillation driven by layer 2/3. It runs using the VERTEX simulator, which is written in Matlab and is available from http://www.vertexsimulator.org
225. Large-scale neural model of visual short-term memory (Ulloa, Horwitz 2016; Horwitz, et al. 2005,...)
Large-scale neural model of visual short term memory embedded into a 998-node connectome. The model simulates electrical activity across neuronal populations of a number of brain regions and converts that activity into fMRI and MEG time-series. The model uses a neural simulator developed at the Brain Imaging and Modeling Section of the National Institutes of Health.
226. Large-scale neuromusculoskeletal model of human upright standing (Elias et al 2014)
" ... This paper studies neuromuscular mechanisms behind upright stance control by means of a biologically based large-scale neuromusculoskeletal (NMS) model. It encompasses: i) conductance-based spinal neuron models (motor neurons and interneurons); ii) muscle proprioceptor models (spindle and Golgi tendon organ) providing sensory afferent feedback; iii) Hill-type muscle models of the leg plantar and dorsiflexors; and iv) an inverted pendulum model for the body biomechanics during upright stance. The motor neuron pools are driven by stochastic spike trains. Simulation results showed that the neuromechanical outputs generated by the NMS model resemble experimental data from subjects standing on a stable surface. ..."
227. Late emergence of the whisker direction selectivity map in rat barrel cortex (Kremer et al. 2011)
"... We discovered that the emergence of a direction map in rat barrel cortex occurs long after all known critical periods in the somatosensory system. This map is remarkably specific, taking a pinwheel-like form centered near the barrel center and aligned to the barrel cortex somatotopy. We suggest that this map may arise from intracortical mechanisms and demonstrate by simulation that the combination of spike-timing-dependent plasticity at synapses between layer 4 and layer 2/3 and realistic pad stimulation is sufficient to produce such a map. ..."
228. Lateral dendrodenditic inhibition in the Olfactory Bulb (David et al. 2008)
Mitral cells, the principal output neurons of the olfactory bulb, receive direct synaptic activation from primary sensory neurons. Shunting inhibitory inputs delivered by granule cell interneurons onto mitral cell lateral dendrites are believed to influence spike timing and underlie coordinated field potential oscillations. Lateral dendritic shunt conductances delayed spiking to a degree dependent on both their electrotonic distance and phase of onset. Recurrent inhibition significantly narrowed the distribution of mitral cell spike times, illustrating a tendency towards coordinated synchronous activity. This result suggests an essential role for early mechanisms of temporal coordination in olfaction. The model was adapted from Davison et al, 2003, but include additional noise mechanisms, long lateral dendrite, and specific synaptic point processes.
229. Learning spatial transformations through STDP (Davison, Frégnac 2006)
A common problem in tasks involving the integration of spatial information from multiple senses, or in sensorimotor coordination, is that different modalities represent space in different frames of reference. Coordinate transformations between different reference frames are therefore required. One way to achieve this relies on the encoding of spatial information using population codes. The set of network responses to stimuli in different locations (tuning curves) constitute a basis set of functions which can be combined linearly through weighted synaptic connections in order to approximate non-linear transformations of the input variables. The question then arises how the appropriate synaptic connectivity is obtained. This model shows that a network of spiking neurons can learn the coordinate transformation from one frame of reference to another, with connectivity that develops continuously in an unsupervised manner, based only on the correlations available in the environment, and with a biologically-realistic plasticity mechanism (spike timing-dependent plasticity).
230. Leech Heart (HE) Motor Neuron conductances contributions to NN activity (Lamb & Calabrese 2013)
"... To explore the relationship between conductances, and in particular how they influence the activity of motor neurons in the well characterized leech heartbeat system, we developed a new multi-compartmental Hodgkin-Huxley style leech heart motor neuron model. To do so, we evolved a population of model instances, which differed in the density of specific conductances, capable of achieving specific output activity targets given an associated input pattern. ... We found that the strengths of many conductances, including those with differing dynamics, had strong partial correlations and that these relationships appeared to be linked by their influence on heart motor neuron activity. Conductances that had positive correlations opposed one another and had the opposite effects on activity metrics when perturbed whereas conductances that had negative correlations could compensate for one another and had similar effects on activity metrics. "
231. Leech Heart Interneuron model (Sharma et al 2020)
Fractional order Leech heart interneuron model is investigated. Different firing properties are explored. In this article, we investigate the alternation of spiking and bursting phenomena of an uncoupled and coupled fractional Leech-Heart (L-H) neurons. We show that a complete graph of heterogeneous de-synchronized neurons in the backdrop of diverse memory settings (a mixture of integer and fractional exponents) can eventually lead to bursting with the formation of cluster synchronization over a certain threshold of coupling strength, however, the uncoupled L-H neurons cannot reveal bursting dynamics. Using the stability analysis in fractional domain, we demarcate the parameter space where the quiescent or steady-state emerges in uncoupled L-H neuron. Finally, a reduced-order model is introduced to capture the activities of the large network of fractional-order model neurons.
232. Leech heart interneuron network model (Hill et al 2001, 2002)
We have created a computational model of the timing network that paces the heartbeat of the medicinal leech, Hirudo medicinalis. In the intact nerve cord, segmental oscillators are mutually entrained to the same cycle period. Although experiments have shown that the segmental oscillators are coupled by inhibitory coordinating interneurons, the underlying mechanisms of intersegmental coordination have not yet been elucidated. To help understand this coordination, we have created a simple computational model with two variants: symmetric and asymmetric. See references for more details. Biologically realistic network models with two, six, and eight cells and a tutorial are available at the links to Calabrese's web site below.
233. LFP signature of monosynaptic thalamocortical connection (Hagen et al 2017)
"A resurgence has taken place in recent years in the use of the extracellularly recorded local field potential (LFP) to investigate neural network activity. To probe monosynaptic thalamic activation of cortical postsynaptic target cells, so called spike-trigger-averaged LFP (stLFP) signatures have been measured. In these experiments, the cortical LFP is measured by multielectrodes covering several cortical lamina and averaged on spontaneous spikes of thalamocortical (TC) cells. Using a well established forward-modeling scheme, we investigated the biophysical origin of this stLFP signature with simultaneous synaptic activation of cortical layer-4 neurons, mimicking the effect of a single afferent spike from a single TC neuron. ..."
234. LGNcircuit: Minimal LGN network model of temporal processing of visual input (Norheim et al. 2012)
The responses of relay cells in the lateral geniculate nucleus (LGN) are shaped by their diverse set of impinging inputs: feedforward synaptic inputs stemming from retina, and feedback inputs stemming from the visual cortex and the thalamic reticular nucleus. This MATLAB model, with an easy-to-use graphical user interface (GUI), explores possible roles of these feedforward and feedback inputs in shaping the temporal part of the receptive fields of LGN relay cells with, so called, ON symmetry. A minimal mechanistic firing-rate model tailored to elucidate salient feedforward and feedback effects is considered including, in particular, feedforward excitation and inhibition (via interneurons) from retinal ON cells and excitatory and inhibitory (via thalamic reticular nucleus cells and interneurons) feedback from cortical ON and OFF cells. Various types of visual stimuli can be explored: flashing spots, impulses, sinusoidal gratings.
235. Linking dynamics of the inhibitory network to the input structure (Komarov & Bazhenov 2016)
Code to model 10 all-to-all coupled inhibitory neurons.
236. Linking STDP and Dopamine action to solve the distal reward problem (Izhikevich 2007)
"... How does the brain know what firing patterns of what neurons are responsible for the reward if 1) the patterns are no longer there when the reward arrives and 2) all neurons and synapses are active during the waiting period to the reward? Here, we show how the conundrum is resolved by a model network of cortical spiking neurons with spike-timing-dependent plasticity (STDP) modulated by dopamine (DA). Although STDP is triggered by nearly coincident firing patterns on a millisecond timescale, slow kinetics of subsequent synaptic plasticity is sensitive to changes in the extracellular DA concentration during the critical period of a few seconds. ... This study emphasizes the importance of precise firing patterns in brain dynamics and suggests how a global diffusive reinforcement signal in the form of extracellular DA can selectively influence the right synapses at the right time." See paper for more and details.
237. Lobster STG pyloric network model with calcium sensor (Gunay & Prinz 2010) (Prinz et al. 2004)
This pyloric network model simulator is a C/C++ program that saves 384 different calcium sensor values that are candidates for activity sensors (Gunay and Prinz, 2010). The simulator was used to scan all of the 20 million pyloric network models that were previously collected in a database (Prinz et al, 2004).
238. Locust olfactory network with GGN and full KC population in the mushroom body (Ray et al 2020)
We reconstructed the GGN (giant GABAergic neuron) morphology from 3D confocal image stack, and built a passive model based on the morphology to study signal attenuation across this giant neuron. In order to study the effect of feedback inhibition from this cell on odor information processing, we created a model of the olfactory network in the locust mushroom body with 50,000 KCs (Kenyon cell) reciprocally connected to this neuron. Finally, we added a model of the IG (Inhibitor of GGN) to reproduce in vivo odor responses in GGN.
239. Logarithmic distributions prove that intrinsic learning is Hebbian (Scheler 2017)
"In this paper, we present data for the lognormal distributions of spike rates, synaptic weights and intrinsic excitability (gain) for neurons in various brain areas, such as auditory or visual cortex, hippocampus, cerebellum, striatum, midbrain nuclei. We find a remarkable consistency of heavy-tailed, specifically lognormal, distributions for rates, weights and gains in all brain areas examined. The difference between strongly recurrent and feed-forward connectivity (cortex vs. striatum and cerebellum), neurotransmitter (GABA (striatum) or glutamate (cortex)) or the level of activation (low in cortex, high in Purkinje cells and midbrain nuclei) turns out to be irrelevant for this feature. Logarithmic scale distribution of weights and gains appears to be a general, functional property in all cases analyzed. We then created a generic neural model to investigate adaptive learning rules that create and maintain lognormal distributions. We conclusively demonstrate that not only weights, but also intrinsic gains, need to have strong Hebbian learning in order to produce and maintain the experimentally attested distributions. This provides a solution to the long-standing question about the type of plasticity exhibited by intrinsic excitability."
240. Long time windows from theta modulated inhib. in entorhinal–hippo. loop (Cutsuridis & Poirazi 2015)
"A recent experimental study (Mizuseki et al., 2009) has shown that the temporal delays between population activities in successive entorhinal and hippocampal anatomical stages are longer (about 70–80 ms) than expected from axon conduction velocities and passive synaptic integration of feed-forward excitatory inputs. We investigate via computer simulations the mechanisms that give rise to such long temporal delays in the hippocampus structures. ... The model shows that the experimentally reported long temporal delays in the DG, CA3 and CA1 hippocampal regions are due to theta modulated somatic and axonic inhibition..."
241. Loss of phase-locking in non-weakly coupled inhib. networks of type-I neurons (Oh and Matveev 2009)
... Here we examine the loss of synchrony caused by an increase in inhibitory coupling in networks of type-I Morris–Lecar model oscillators, which is characterized by a period-doubling cascade and leads to mode-locked states with alternation in the firing order of the two cells, as reported recently by Maran and Canavier (J Comput Nerosci, 2008) for a network of Wang-Buzsáki model neurons. Although alternating-order firing has been previously reported as a near-synchronous state, we show that the stable phase difference between the spikes of the two Morris–Lecar cells can constitute as much as 70% of the unperturbed oscillation period. Further, we examine the generality of this phenomenon for a class of type-I oscillators that are close to their excitation thresholds, and provide an intuitive geometric description of such “leap-frog” dynamics. ..."
242. Maximum entropy model to predict spatiotemporal spike patterns (Marre et al. 2009)
This MATLAB code implements a model-based analysis of spike trains. The analysis predicts the occurrence of spatio-temporal patterns of spikes in the data, and is based on a maximum entropy principle by including both spatial and temporal correlations. The approach is applicable to unit recordings from any region of the brain. The code is based on Marre, et al., 2009. The MATLAB code was written by Sami El Boustani and Olivier Marre.
243. MDD: the role of glutamate dysfunction on Cingulo-Frontal NN dynamics (Ramirez-Mahaluf et al 2017)
" ...Currently, no mechanistic framework describes how network dynamics, glutamate, and serotonin interact to explain MDD symptoms and treatments. Here, we built a biophysical computational model of 2 areas (vACC and dlPFC) that can switch between emotional and cognitive processing. (Major Depression Disease) MDD networks were simulated by slowing glutamate decay in vACC and demonstrated sustained vACC activation. ..."
244. Mean Field Equations for Two-Dimensional Integrate and Fire Models (Nicola and Campbell, 2013)
The zip file contains the files used to perform numerical simulation and bifurcation studies of large networks of two-dimensional integrate and fire neurons and of the corresponding mean field models derived in our paper. The neural models used are the Izhikevich model and the Adaptive Exponential model.
245. Mean-field models of neural populations under electrical stimulation (Cakan & Obermayer 2020)
Weak electrical inputs to the brain in vivo using transcranial electrical stimulation or in isolated cortex in vitro can affect the dynamics of the underlying neural populations. However, it is poorly understood what the exact mechanisms are that modulate the activity of neural populations as a whole and why the responses are so diverse in stimulation experiments. Despite this, electrical stimulation techniques are being developed for the treatment of neurological diseases in humans. To better understand these interactions, it is often necessary to simulate and analyze very large networks of neurons, which can be computationally demanding. In this theoretical paper, we present a reduced model of coupled neural populations that represents a piece of cortical tissue. This efficient model retains the dynamical properties of the large network of neurons it is based on while being several orders of magnitude faster to simulate. Due to the biophysical properties of the neuron model, an electric field can be coupled to the population. We show that weak electric fields often used in stimulation experiments can lead to entrainment of neural oscillations on the population level, and argue that the responses critically depend on the dynamical state of the neural system.
246. Mechanisms for stable, robust, and adaptive development of orientation maps (Stevens et al. 2013)
GCAL (Gain Control, Adaptation, Laterally connected). Simple but robust single-population V1 orientation map model.
247. Mechanisms of very fast oscillations in axon networks coupled by gap junctions (Munro, Borgers 2010)
Axons connected by gap junctions can produce very fast oscillations (VFOs, > 80 Hz) when stimulated randomly at a low rate. The models here explore the mechanisms of VFOs that can be seen in an axonal plexus, (Munro & Borgers, 2009): a large network model of an axonal plexus, small network models of axons connected by gap junctions, and an implementation of the model underlying figure 12 in Traub et al. (1999) . The large network model consists of 3,072 5-compartment axons connected in a random network. The 5-compartment axons are the 5 axonal compartments from the CA3 pyramidal cell model in Traub et al. (1994) with a fixed somatic voltage. The random network has the same parameters as the random network in Traub et al. (1999), and axons are stimulated randomly via a Poisson process with a rate of 2/s/axon. The small network models simulate waves propagating through small networks of axons connected by gap junctions to study how local connectivity affects the refractory period.
248. Medial reticular formation of the brainstem: anatomy and dynamics (Humphries et al. 2006, 2007)
A set of models to study the medial reticular formation (mRF) of the brainstem. We developed a collection of algorithms to derive the adult-state wiring of the model: one set a stochastic model; the other set mimicking the developmental process. We found that the anatomical models had small-world properties, irrespective of the choice of algorithm; and that the cluster-like organisation of the mRF may have arisen to minimise wiring costs. (The model code includes options to be run as dynamic models; papers examining these dynamics are included in the .zip file).
249. MEG of Somatosensory Neocortex (Jones et al. 2007)
"... To make a direct and principled connection between the SI (somatosensory primary neocortex magnetoencephalography) waveform and underlying neural dynamics, we developed a biophysically realistic computational SI model that contained excitatory and inhibitory neurons in supragranular and infragranular layers. ... our model provides a biophysically realistic solution to the MEG signal and can predict the electrophysiological correlates of human perception."
250. Mesoscopic dynamics from AdEx recurrent networks (Zerlaut et al JCNS 2018)
We present a mean-field model of networks of Adaptive Exponential (AdEx) integrate-and-fire neurons, with conductance-based synaptic interactions. We study a network of regular-spiking (RS) excitatory neurons and fast-spiking (FS) inhibitory neurons. We use a Master Equation formalism, together with a semi-analytic approach to the transfer function of AdEx neurons to describe the average dynamics of the coupled populations. We compare the predictions of this mean-field model to simulated networks of RS-FS cells, first at the level of the spontaneous activity of the network, which is well predicted by the analytical description. Second, we investigate the response of the network to time-varying external input, and show that the mean-field model predicts the response time course of the population. Finally, to model VSDi signals, we consider a one-dimensional ring model made of interconnected RS-FS mean-field units.
251. Mesoscopic dynamics from AdEx recurrent networks (Zerlaut et al JCNS 2018) (PyNN)
PyNN simulations for Zerlaut et al 2018).
252. Microcircuits of L5 thick tufted pyramidal cells (Hay & Segev 2015)
"... We simulated detailed conductance-based models of TTCs (Layer 5 thick tufted pyramidal cells) forming recurrent microcircuits that were interconnected as found experimentally; the network was embedded in a realistic background synaptic activity. ... Our findings indicate that dendritic nonlinearities are pivotal in controlling the gain and the computational functions of TTCs microcircuits, which serve as a dominant output source for the neocortex. "
253. Minimal model of interictal and ictal discharges “Epileptor-2” (Chizhov et al 2018)
"Seizures occur in a recurrent manner with intermittent states of interictal and ictal discharges (IIDs and IDs). The transitions to and from IDs are determined by a set of processes, including synaptic interaction and ionic dynamics. Although mathematical models of separate types of epileptic discharges have been developed, modeling the transitions between states remains a challenge. A simple generic mathematical model of seizure dynamics (Epileptor) has recently been proposed by Jirsa et al. (2014); however, it is formulated in terms of abstract variables. In this paper, a minimal population-type model of IIDs and IDs is proposed that is as simple to use as the Epileptor, but the suggested model attributes physical meaning to the variables. The model is expressed in ordinary differential equations for extracellular potassium and intracellular sodium concentrations, membrane potential, and short-term synaptic depression variables. A quadratic integrate-and-fire model driven by the population input current is used to reproduce spike trains in a representative neuron. ..."
254. Mitral cell activity gating by respiration and inhibition in an olfactory bulb NN (Short et al 2016)
To explore interactions between respiration, inhibition, and olfaction, experiments using light to active channel rhodopsin in sensory neurons expressing Olfactory Marker Protein were performed in mice and modeled in silico. This archive contains NEURON models that were run on parallel computers to explore the interactions between varying strengths of respiratory activity and olfactory sensory neuron input and the roles of periglomerular, granule, and external tufted cells in shaping mitral cell responses.
255. Model of arrhythmias in a cardiac cells network (Casaleggio et al. 2014)
" ... Here we explore the possible processes leading to the occasional onset and termination of the (usually) non-fatal arrhythmias widely observed in the heart. Using a computational model of a two-dimensional network of cardiac cells, we tested the hypothesis that an ischemia alters the properties of the gap junctions inside the ischemic area. ... In conclusion, our model strongly supports the hypothesis that non-fatal arrhythmias can develop from post-ischemic alteration of the electrical connectivity in a relatively small area of the cardiac cell network, and suggests experimentally testable predictions on their possible treatments."
256. Model of CA1 activity during working memory task (Spera et al. 2016)
"The cellular processes underlying individual differences in the Woring Memory Capacity (WMC) of humans are essentially unknown. Psychological experiments suggest that subjects with lower working memory capacity (LWMC), with respect to subjects with higher capacity (HWMC), take more time to recall items from a list because they search through a larger set of items and are much more susceptible to interference during retrieval. ... In this paper, we investigate the possible underlying mechanisms at the single neuron level by using a computational model of hippocampal CA1 pyramidal neurons, which have been suggested to be deeply involved in the recognition of specific items. ..."
257. Model of eupnea and sigh generation in respiratory network (Toporikova et al 2015)
Based on recent in vitro data obtained in the mouse embryo, we have built a computational model consisting of two compartments, interconnected through appropriate synapses. One compartment generates sighs and the other produces eupneic bursts. The model reproduces basic features of simultaneous sigh and eupnea generation (two types of bursts differing in terms of shape, amplitude, and frequency of occurrence) and mimics the effect of blocking glycinergic synapses
258. Model of long range transmission of gamma oscillation (Murray 2007)
"... A minimal mathematical model was developed for a preliminary study of long-range neural transmission of gamma oscillation from the CA3 to the entorhinal cortex via the CAI region of the hippocampus, a subset within a larger complex set of pathways. A module was created for each local population of neurons with common intrinsic properties and connectivity to simplify the connection process and make the model more flexible. Three modules were created using MATLAB Simulink® and tested to confirm that they transmit gamma through the system. The model also revealed that a portion of the signal from CAI to the entorhinal cortex may be lost in transmission under certain conditions."
259. Model of memory linking through memory allocation (Kastellakis et al. 2016)
Here, we present a simplified, biophysically inspired network model that incorporates multiple plasticity processes and explains linking of information at three different levels: (a) learning of a single associative memory (b) rescuing of a weak memory when paired with a strong one and (c) linking of multiple memories across time. By dissecting synaptic from intrinsic plasticity and neuron-wide from dendritically restricted protein capture, the model reveals a simple, unifying principle: Linked memories share synaptic clusters within the dendrites of overlapping populations of neurons
260. Model of the cerebellar granular network (Sudhakar et al 2017)
"The granular layer, which mainly consists of granule and Golgi cells, is the first stage of the cerebellar cortex and processes spatiotemporal information transmitted by mossy fiber inputs with a wide variety of firing patterns. To study its dynamics at multiple time scales in response to inputs approximating real spatiotemporal patterns, we constructed a large-scale 3D network model of the granular layer. ..."
261. Model of working memory based on negative derivative feedback (Lim and Goldman, 2013)
We proposed a model of working memory in which recurrent synaptic interactions provide a corrective feedback that enables persistent activity to be maintained stably for prolonged durations. When recurrent excitatory and inhibitory inputs to memory neurons were balanced in strength and offset in time, drifts in activity triggered a corrective signal that counteracted memory decay. Circuits containing this mechanism temporally integrated their inputs, generated the irregular neural firing observed during persistent activity and were robust against common perturbations that severely disrupted previous models of short-term memory storage.
262. Modeling and MEG evidence of early consonance processing in auditory cortex (Tabas et al 2019)
Pitch is a fundamental attribute of auditory perception. The interaction of concurrent pitches gives rise to a sensation that can be characterized by its degree of consonance or dissonance. In this work, we propose that human auditory cortex (AC) processes pitch and consonance through a common neural network mechanism operating at early cortical levels. First, we developed a new model of neural ensembles incorporating realistic neuronal and synaptic parameters to assess pitch processing mechanisms at early stages of AC. Next, we designed a magnetoencephalography (MEG) experiment to measure the neuromagnetic activity evoked by dyads with varying degrees of consonance or dissonance. MEG results show that dissonant dyads evoke a pitch onset response (POR) with a latency up to 36 ms longer than consonant dyads. Additionally, we used the model to predict the processing time of concurrent pitches; here, consonant pitch combinations were decoded faster than dissonant combinations, in line with the experimental observations. Specifically, we found a striking match between the predicted and the observed latency of the POR as elicited by the dyads. These novel results suggest that consonance processing starts early in human auditory cortex and may share the network mechanisms that are responsible for (single) pitch processing.
263. Modeling dendritic spikes and plasticity (Bono and Clopath 2017)
Biophysical model and reduced neuron model with voltage-dependent plasticity.
264. Modeling epileptic seizure induced by depolarization block (Kim & Dykamp 2017)
"The inhibitory restraint necessary to suppress aberrant activity can fail when inhibitory neurons cease to generate action potentials as they enter depolarization block. We investigate possible bifurcation structures that arise at the onset of seizure-like activity resulting from depolarization block in inhibitory neurons. Networks of conductance based excitatory and inhibitory neurons are simulated to characterize different types of transitions to the seizure state, and a mean field model is developed to verify the generality of the observed phenomena of excitatory-inhibitory dynamics. ..."
265. Modeling hebbian and homeostatic plasticity (Toyoizumi et al. 2014)
"... We propose a model in which synaptic strength is the product of a synapse-specific Hebbian factor and a postsynaptic- cell-specific homeostatic factor, with each factor separately arriving at a stable inactive state. This model captures ODP dynamics and has plausible biophysical substrates. We confirm model predictions experimentally that plasticity is inactive at stable states and that synaptic strength overshoots during recovery from visual deprivation. ..."
266. Modeling the effects of dopamine on network synchronization (Komek et al. 2012)
Dopamine modulates cortical circuit activity in part through its actions on GABAergic interneurons, including increasing the excitability of fast-spiking interneurons. Though such effects have been demonstrated in single cells, there are no studies that examine how such mechanisms may lead to the effects of dopamine at a neural network level. In this study, we investigated the effects of dopamine on synchronization in two simulated neural networks; one biophysical model composed of Wang-Buzsaki neurons and a reduced model with theta neurons. In both models, we show that parametrically varying the levels of dopamine, modeled through the changes in the excitability of interneurons, reveals an inverted-U shaped relationship, with low gamma band power at both low and high dopamine levels and optimal synchronization at intermediate levels. Moreover, such a relationship holds when the external input is both tonic and periodic at gamma band range. Together, our results indicate that dopamine can modulate cortical gamma band synchrony in an inverted-U fashion and that the physiologic effects of dopamine on single fast-spiking interneurons can give rise to such non-monotonic effects at the network level.
267. Modelling enteric neuron populations and muscle fed-state motor patterns (Chambers et al. 2011)
"After a meal, the gastrointestinal tract exhibits a set of behaviours known as the fed state. ... Segmentation manifests as rhythmic local constrictions that do not propagate along the intestine. ... We investigated the enteric circuits that regulate segmentation focusing on a central feature of the ENS: a recurrent excitatory network of intrinsic sensory neurons (ISNs) which are characterized by prolonged after-hyperpolarizing potentials (AHPs) following their action potentials. ..."
268. Modelling platform of the cochlear nucleus and other auditory circuits (Manis & Compagnola 2018)
"Models of the auditory brainstem have been an invaluable tool for testing hypotheses about auditory information processing and for highlighting the most important gaps in the experimental literature. Due to the complexity of the auditory brainstem, and indeed most brain circuits, the dynamic behavior of the system may be difficult to predict without a detailed, biologically realistic computational model. Despite the sensitivity of models to their exact construction and parameters, most prior models of the cochlear nucleus have incorporated only a small subset of the known biological properties. This confounds the interpretation of modelling results and also limits the potential future uses of these models, which require a large effort to develop. To address these issues, we have developed a general purpose, bio-physically detailed model of the cochlear nucleus for use both in testing hypotheses about cochlear nucleus function and also as an input to models of downstream auditory nuclei. The model implements conductance-based Hodgkin-Huxley representations of cells using a Python-based interface to the NEURON simulator. ..."
269. Models for cortical UP-DOWN states in a bistable inhibitory-stabilized network (Jercog et al 2017)
In the idling brain, neuronal circuits transition between periods of sustained firing (UP state) and quiescence (DOWN state), a pattern the mechanisms of which remain unclear. We analyzed spontaneous cortical population activity from anesthetized rats and found that UP and DOWN durations were highly variable and that population rates showed no significant decay during UP periods. We built a network rate model with excitatory (E) and inhibitory (I) populations exhibiting a novel bistable regime between a quiescent and an inhibition-stabilized state of arbitrarily low rate, where fluctuations triggered state transitions. In addition, we implemented these mechanisms in a more biophysically realistic spiking network, where DOWN-to-UP transitions are caused by synchronous high-amplitude events impinging onto the network.
270. Models of Vector Navigation with Grid Cells (Bush et al., 2015)
Four models of vector navigation in large scale 2D space using grid cell representations of location are included: (1) The 'Distance Cell' model, which directly decodes absolute start and goal locations in allocentric space from rate-coded grid cell representations before computing the displacement between them; (2) The 'Rate-coded Vector Cell' model, which directly decodes the displacement between start and goal locations from rate-coded grid cell representations; (3) The 'Phase-coded Vector Cell' model, which directly decodes the displacement between start and goal locations from the temporally-coded grid cell representations provided by phase precession; (4) The 'Linear Look-ahead' model, which uses a directed search through grid cell representations, initiated at the start location and then moving along a specific axis at a constant speed, to compute the displacement between start and goal locations.
271. Modular grid cell responses as a basis for hippocampal remapping (Monaco and Abbott 2011)
"Hippocampal place fields, the local regions of activity recorded from place cells in exploring rodents, can undergo large changes in relative location during remapping. This process would appear to require some form of modulated global input. Grid-cell responses recorded from layer II of medial entorhinal cortex in rats have been observed to realign concurrently with hippocampal remapping, making them a candidate input source. However, this realignment occurs coherently across colocalized ensembles of grid cells (Fyhn et al., 2007). The hypothesized entorhinal contribution to remapping depends on whether this coherence extends to all grid cells, which is currently unknown. We study whether dividing grid cells into small numbers of independently realigning modules can both account for this localized coherence and allow for hippocampal remapping. ..."
272. Modulation of hippocampal rhythms by electric fields and network topology (Berzhanskaya et al. 2013)
“… Here we present experimental and computational evidence of the interplay among hippocampal synaptic circuitry, neuronal morphology, external electric fields, and network activity. Electrophysiological data are used to constrain and validate an anatomically and biophysically realistic model of area CA1 containing pyramidal cells and two interneuron types: dendritic- and perisomatic-targeting. We report two lines of results: addressing the network structure capable of generating theta-modulated gamma rhythms, and demonstrating electric field effects on those rhythms. First, theta-modulated gamma rhythms require specific inhibitory connectivity. … The second major finding is that subthreshold electric fields robustly alter the balance between different rhythms. …”
273. Modulation of septo-hippocampal theta activity by GABAA receptors (Hajos et al. 2004)
Theta frequency oscillation of the septo-hippocampal system has been considered as a prominent activity associated with cognitive function and affective processes. ... In the present experiments we applied a combination of computational and physiological techniques to explore the functional role of GABAA receptors in theta oscillation. ... In parallel to these experimental observations, a computational model has been constructed by implementing a septal GABA neuron model with a CA1 hippocampal model containing three types of neurons (including oriens and basket interneurons and pyramidal cells; latter modeled by multicompartmental techniques; for detailed model description with network parameters see online addendum: http://geza.kzoo.edu/theta). This connectivity made the network capable of simulating the responses of the septo-hippocampal circuitry to the modulation of GABAA transmission, and the presently described computational model proved suitable to reveal several aspects of pharmacological modulation of GABAA receptors. In addition, computational findings indicated different roles of distinctively located GABAA receptors in theta generation.
274. Motor cortex microcircuit simulation based on brain activity mapping (Chadderdon et al. 2014)
"... We developed a computational model based primarily on a unified set of brain activity mapping studies of mouse M1. The simulation consisted of 775 spiking neurons of 10 cell types with detailed population-to-population connectivity. Static analysis of connectivity with graph-theoretic tools revealed that the corticostriatal population showed strong centrality, suggesting that would provide a network hub. ... By demonstrating the effectiveness of combined static and dynamic analysis, our results show how static brain maps can be related to the results of brain activity mapping."
275. Motor system model with reinforcement learning drives virtual arm (Dura-Bernal et al 2017)
"We implemented a model of the motor system with the following components: dorsal premotor cortex (PMd), primary motor cortex (M1), spinal cord and musculoskeletal arm (Figure 1). PMd modulated M1 to select the target to reach, M1 excited the descending spinal cord neurons that drove the arm muscles, and received arm proprioceptive feedback (information about the arm position) via the ascending spinal cord neurons. The large-scale model of M1 consisted of 6,208 spiking Izhikevich model neurons [37] of four types: regular-firing and bursting pyramidal neurons, and fast-spiking and low-threshold-spiking interneurons. These were distributed across cortical layers 2/3, 5A, 5B and 6, with cell properties, proportions, locations, connectivity, weights and delays drawn primarily from mammalian experimental data [38], [39], and described in detail in previous work [29]. The network included 486,491 connections, with synapses modeling properties of four different receptors ..."
276. Multi-area layer-resolved spiking network model of resting-state dynamics in macaque visual cortex
See https://inm-6.github.io/multi-area-model/ for any updates.
277. Multiplication by NMDA receptors in Direction Selective Ganglion cells (Poleg-Polsky & Diamond 2016)
The model demonstrates how signal amplification with NMDARs depends on the synaptic environment. When direction selectivity (DS) detection is mediated by DS inhibition, NMDARs multiply other synaptic conductances. In the case of DS tuned excitation, NMDARs contribute additively.
278. Multiscale model of excitotoxicity in PD (Muddapu and Chakravarthy 2020)
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in Substantia Nigra pars compacta (SNc). Although the exact cause of cell death is not clear, the hypothesis that metabolic deficiency is a key factor has been gaining attention in recent years. In the present study, we investigate this hypothesis using a multi-scale computational model of the subsystem of the basal ganglia comprising Subthalamic Nucleus (STN), Globus Pallidus externa (GPe) and SNc. The proposed model is a multiscale model in that interactions among the three nuclei are simulated using more abstract Izhikevich neuron models, while the molecular pathways involved in cell death of SNc neurons are simulated in terms of detailed chemical kinetics. Simulation results obtained from the proposed model showed that energy deficiencies occurring at cellular and network levels could precipitate the excitotoxic loss of SNc neurons in PD. At the subcellular level, the models show how calcium elevation leads to apoptosis of SNc neurons. The therapeutic effects of several neuroprotective interventions are also simulated in the model. From neuroprotective studies, it was clear that glutamate inhibition and apoptotic signal blocker therapies were able to halt the progression of SNc cell loss when compared to other therapeutic interventions, which only slows down the progression of SNc cell loss.
279. Multisensory integration in the superior colliculus: a neural network model (Ursino et al. 2009)
" ... The model includes three distinct neural areas: two unimodal areas (auditory and visual) are devoted to a topological representation of external stimuli, and communicate via synaptic connections with a third downstream area (in the SC) responsible for multisensory integration. The present simulations show that the model, with a single set of parameters, can mimic various responses to different combinations of external stimuli including the inverse effectiveness, both in terms of multisensory enhancement and contrast, the existence of within- and cross-modality suppression between spatially disparate stimuli, a reduction of network settling time in response to cross-modal stimuli compared with individual stimuli. ..."
280. Multistability of clustered states in a globally inhibitory network (Chandrasekaran et al. 2009)
"We study a network of m identical excitatory cells projecting excitatory synaptic connections onto a single inhibitory interneuron, which is reciprocally coupled to all excitatory cells through inhibitory synapses possessing short-term synaptic depression. We find that such a network with global inhibition possesses multiple stable activity patterns with distinct periods, characterized by the clustering of the excitatory cells into synchronized sub-populations. We prove the existence and stability of n-cluster solutions in a m-cell network. ... Implications for temporal coding and memory storage are discussed."
281. Multitarget pharmacology for Dystonia in M1 (Neymotin et al 2016)
" ... We developed a multiscale model of primary motor cortex, ranging from molecular, up to cellular, and network levels, containing 1715 compartmental model neurons with multiple ion channels and intracellular molecular dynamics. We wired the model based on electrophysiological data obtained from mouse motor cortex circuit mapping experiments. We used the model to reproduce patterns of heightened activity seen in dystonia by applying independent random variations in parameters to identify pathological parameter sets. ..."
282. Muscle spindle feedback circuit (Moraud et al, 2016)
Here, we developed a computational model of the muscle spindle feedback circuits of the rat ankle that predicts the interactions between Epidural Stimulation and spinal circuit dynamics during gait.
283. Na channel mutations in the dentate gyrus (Thomas et al. 2009)
These are source files to generate the data in Figure 6 from "Mossy fiber sprouting interacts with sodium channel mutations to increase dentate gyrus excitability" Thomas EA, Reid CA, Petrou S, Epilepsia (2009)
284. Neocort. pyramidal cells subthreshold somatic voltage controls spike propagation (Munro Kopell 2012)
There is suggestive evidence that pyramidal cell axons in neocortex may be coupled by gap junctions into an ``axonal plexus" capable of generating Very Fast Oscillations (VFOs) with frequencies exceeding 80 Hz. It is not obvious, however, how a pyramidal cell in such a network could control its output when action potentials are free to propagate from the axons of other pyramidal cells into its own axon. We address this problem by means of simulations based on 3D reconstructions of pyramidal cells from rat somatosensory cortex. We show that somatic depolarization enables propagation via gap junctions into the initial segment and main axon, while somatic hyperpolarization disables it. We show further that somatic voltage cannot effectively control action potential propagation through gap junctions on minor collaterals; action potentials may therefore propagate freely from such collaterals regardless of somatic voltage. In previous work, VFOs are all but abolished during the hyperpolarization phase of slow-oscillations induced by anesthesia in vivo. This finding constrains the density of gap junctions on collaterals in our model and suggests that axonal sprouting due to cortical lesions may result in abnormally high gap junction density on collaterals, leading in turn to excessive VFO activity and hence to epilepsy via kindling.
285. NETMORPH: creates NNs with realistic neuron morphologies (Koene et al. 2009, van Ooyen et al. 2014)
NETMORPH is a simulation tool for building synaptically connected networks with realistic neuron morphologies. Axonal and dendritic morphologies are created by using stochastic rules for the behavior of individual growth cones, the structures at the tip of outgrowing axons and dendrites that mediate elongation and branching. Axons and dendrites are not guided by any extracellular cues. Synapses are formed when crossing axonal and dendritic segments come sufficiently close to each other. See the README in the archive for more information.
286. Network bursts in cultured NN result from different adaptive mechanisms (Masquelier & Deco 2013)
It is now well established that cultured neuron networks are spontaneously active, and tend to synchronize. Synchronous events typically involve the whole network, and have thus been termed “network spikes” (NS). Using experimental recordings and numerical simulations, we show here that the inter-NS interval statistics are complex, and allow inferring the neural mechanisms at work, in particular the adaptive ones, and estimating a number of parameters to which we cannot access experimentally.
287. Network model of the granular layer of the cerebellar cortex (Maex, De Schutter 1998)
We computed the steady-state activity of a large-scale model of the granular layer of the rat cerebellum. Within a few tens of milliseconds after the start of random mossy fiber input, the populations of Golgi and granule cells became entrained in a single synchronous oscillation, the basic frequency of which ranged from 10 to 40 Hz depending on the average rate of firing in the mossy fiber population. ... The synchronous, rhythmic firing pattern was robust over a broad range of biologically realistic parameter values and to parameter randomization. Three conditions, however, made the oscillations more transient and could desynchronize the entire network in the end: a very low mossy fiber activity, a very dominant excitation of Golgi cells through mossy fiber synapses (rather than through parallel fiber synapses), and a tonic activation of granule cell GABAA receptors (with an almost complete absence of synaptically induced inhibitory postsynaptic currents). The model predicts that, under conditions of strong mossy fiber input to the cerebellum, Golgi cells do not only control the strength of parallel fiber activity but also the timing of the individual spikes. Provided that their parallel fiber synapses constitute an important source of excitation, Golgi cells fire rhythmically and synchronized with granule cells over large distances along the parallel fiber axis. See paper for more and details.
288. Network model with dynamic ion concentrations (Ullah et al. 2009)
This is a network model composed of 100 excitatory and 100 inhibitory neurons with dynamic ion concentrations as described in "The Influence of Sodium and Potassium Dynamics on Excitability, Seizures, and the Stability of Persistent States: II. Network and Glia Dynamics (2009) Journal of Computational Neuroscience, 26:171-183".
289. Network model with neocortical architecture (Anderson et al 2007,2012; Azhar et al 2012)
Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. This is an addendum to ModelDB Accession # 98902, Studies of stimulus parameters for seizure disruption (Anderson et al. 2007). Wiring is adapted from the minicolumn hypothesis and incorporates visual and neocortical wiring data. Simulation demonstrates spontaneous bursting onset and cessation. This activity can be induced by random fluctuations in the surrounding background input.
290. Network models of frequency modulated sweep detection (Skorheim et al. 2014)
"Frequency modulated (FM) sweeps are common in species-specific vocalizations, including human speech. Auditory neurons selective for the direction and rate of frequency change in FM sweeps are present across species, but the synaptic mechanisms underlying such selectivity are only beginning to be understood. Even less is known about mechanisms of experience-dependent changes in FM sweep selectivity. We present three network models of synaptic mechanisms of FM sweep direction and rate selectivity that explains experimental data ... "
291. Network recruitment to coherent oscillations in a hippocampal model (Stacey et al. 2011)
"... Here we demonstrate, via a detailed computational model, a mechanism whereby physiological noise and coupling initiate oscillations and then recruit neighboring tissue, in a manner well described by a combination of Stochastic Resonance and Coherence Resonance. We develop a novel statistical method to quantify recruitment using several measures of network synchrony. This measurement demonstrates that oscillations spread via preexisting network connections such as interneuronal connections, recurrent synapses, and gap junctions, provided that neighboring cells also receive sufficient inputs in the form of random synaptic noise. ..."
292. Network topologies for producing limited sustained activation (Kaiser and Hilgetag 2010)
Uses networks of cellular automata to test hypotheses about network topologies that can produce limited, sustained activity. Inspired by empirically-based ideas about neocortical architecture, but conceived and implemented at a level of abstraction that is not closely linked to empirical observations.
293. Networks of spiking neurons: a review of tools and strategies (Brette et al. 2007)
This package provides a series of codes that simulate networks of spiking neurons (excitatory and inhibitory, integrate-and-fire or Hodgkin-Huxley type, current-based or conductance-based synapses; some of them are event-based). The same networks are implemented in different simulators (NEURON, GENESIS, NEST, NCS, CSIM, XPP, SPLIT, MVAspike; there is also a couple of implementations in SciLab and C++). The codes included in this package are benchmark simulations; see the associated review paper (Brette et al. 2007). The main goal is to provide a series of benchmark simulations of networks of spiking neurons, and demonstrate how these are implemented in the different simulators overviewed in the paper. See also details in the enclosed file Appendix2.pdf, which describes these different benchmarks. Some of these benchmarks were based on the Vogels-Abbott model (Vogels TP and Abbott LF 2005).
294. Neural Interactome: interactive simulation of a neuronal system (Kim et al 2019)
""Connectivity and biophysical processes determine the functionality of neuronal networks. We, therefore, developed a real-time framework, called Neural Interactome, to simultaneously visualize and interact with the structure and dynamics of such networks. Neural Interactome is a cross-platform framework, which combines graph visualization with the simulation of neural dynamics, or experimentally recorded multi neural time series, to allow application of stimuli to neurons to examine network responses. In addition, Neural Interactome supports structural changes, such as disconnection of neurons from the network (ablation feature). Neural dynamics can be explored on a single neuron level (using a zoom feature), back in time (using a review feature), and recorded (using presets feature). The development of the Neural Interactome was guided by generic concepts to be applicable to neuronal networks with different neural connectivity and dynamics. We implement the framework using a model of the nervous system of Caenorhabditis elegans (C. elegans) nematode, a model organism with resolved connectome and neural dynamics. We show that Neural Interactome assists in studying neural response patterns associated with locomotion and other stimuli. In particular, we demonstrate how stimulation and ablation help in identifying neurons that shape particular dynamics. We examine scenarios that were experimentally studied, such as touch response circuit, and explore new scenarios that did not undergo elaborate experimental studies."
295. Neural mass model based on single cell dynamics to model pathophysiology (Zandt et al 2014)
The model code as described in "A neural mass model based on single cell dynamics to model pathophysiology, Zandt et al. 2014, Journal of Computational Neuroscience" A Neural mass model (NMM) derived from single cell dynamics in a bottom up approach. Mean and standard deviation of the firing rates in the populations are calculated. The sigmoid is derived from the single cell FI-curve, allowing for easy implementation of pathological conditions. NMM is compared with a detailed spiking network model consisting of HH neurons. NMM code in Matlab. The network model is simulated using Norns (ModelDB # 154739)
296. Neural model of frog ventilatory rhythmogenesis (Horcholle-Bossavit and Quenet 2009)
"In the adult frog respiratory system, periods of rhythmic movements of the buccal floor are interspersed by lung ventilation episodes. The ventilatory activity results from the interaction of two hypothesized oscillators in the brainstem. Here, we model these oscillators with two coupled neural networks, whose co-activation results in the emergence of new dynamics. .. The biological interest of this formal model is illustrated by the persistence of the relevant dynamical features when perturbations are introduced in the model, i.e. dynamic noises and architecture modifications. The implementation of the networks with clock-driven continuous time neurones provides simulations with physiological time scales."
297. Neural modeling of an internal clock (Yamazaki and Tanaka 2008)
"We studied a simple random recurrent inhibitory network. Despite its simplicity, the dynamics was so rich that activity patterns of neurons evolved with time without recurrence due to random recurrent connections among neurons. The sequence of activity patterns was generated by the trigger of an external signal, and the generation was stable against noise.... Therefore, a time passage from the trigger of an external signal could be represented by the sequence of activity patterns, suggesting that this model could work as an internal clock. ..."
298. Neural transformations on spike timing information (Tripp and Eliasmith 2007)
" ... Here we employ computational methods to show that an ensemble of neurons firing at a constant mean rate can induce arbitrarily chosen temporal current patterns in postsynaptic cells. ..."
299. Neurogenesis in the olfactory bulb controlled by top-down input (Adams et al 2018)
This code implements a model for adult neurogenesis of granule cells in the olfactory system. The granule cells receive sensory input via the mitral cells and top-down input from a cortical area. That cortical area also receives olfactory input from the mitral cells as well as contextual input. This plasticity leads to a network structure consisting of bidirectional connections between bulbar and cortical odor representations. The top-down input enhances stimulus discrimination based on contextual input.
300. Neuromorphic muscle spindle model (Vannucci et al 2017)
A fully spike-based, biologically inspired mechanism for the translation of proprioceptive feedback.
301. Neuron-based control mechanisms for a robotic arm and hand (Singh et al 2017)
"A robotic arm and hand controlled by simulated neurons is presented. The robot makes use of a biological neuron simulator using a point neural model. ... The robot performs a simple pick-and-place task. ... As another benefit, it is hoped that further work will also lead to a better understanding of human and other animal neural processing, particularly for physical motion. This is a multidisciplinary approach combining cognitive neuroscience, robotics, and psychology."
302. Neuronify: An Educational Simulator for Neural Circuits (Dragly et al 2017)
"Neuronify, a new educational software application (app) providing an interactive way of learning about neural networks, is described. Neuronify allows students with no programming experience to easily build and explore networks in a plug-and-play manner picking network elements (neurons, stimulators, recording devices) from a menu. The app is based on the commonly used integrate-and-fire type model neuron and has adjustable neuronal and synaptic parameters. ..."
303. NMDAR & GABAB/KIR Give Bistable Dendrites: Working Memory & Sequence Readout (Sanders et al., 2013)
" ...Here, we show that the voltage dependence of the inwardly rectifying potassium (KIR) conductance activated by GABA(B) receptors adds substantial robustness to network simulations of bistability and the persistent firing that it underlies. The hyperpolarized state is robust because, at hyperpolarized potentials, the GABA(B)/KIR conductance is high and the NMDA conductance is low; the depolarized state is robust because, at depolarized potentials, the NMDA conductance is high and the GABA(B)/KIR conductance is low. Our results suggest that this complementary voltage dependence of GABA(B)/KIR and NMDA conductances makes them a "perfect couple" for producing voltage bistability."
304. Noise promotes independent control of gamma oscillations and grid firing (Solanka et al 2015)
"Neural computations underlying cognitive functions require calibration of the strength of excitatory and inhibitory synaptic connections and are associated with modulation of gamma frequency oscillations in network activity. However, principles relating gamma oscillations, synaptic strength and circuit computations are unclear. We address this in attractor network models that account for grid firing and theta-nested gamma oscillations in the medial entorhinal cortex. ..."
305. Nonlinear dendritic processing in barrel cortex spiny stellate neurons (Lavzin et al. 2012)
This is a multi-compartmental simulation of a spiny stellate neuron which is stimulated by a thalamocortical (TC) and cortico-cortical (CC) inputs. No other cells are explicitly modeled; the presynaptic network activation is represented by the number of active synapses. Preferred and non –preferred thalamic directions thus correspond to larder/smaller number of TC synapses. This simulation revealed that randomly activated synapses can cooperatively trigger global NMDA spikes, which involve participation of most of the dendritic tree. Surprisingly, we found that although the voltage profile of the cell was uniform, the calcium influx was restricted to ‘hot spots’ which correspond to synaptic clusters or large conductance synapses
306. Normal ripples, abnormal ripples, and fast ripples in a hippocampal model (Fink et al. 2015)
"...We use a computational model of hippocampus to investigate possible network mechanisms underpinning normal ripples, pathological ripples, and fast ripples. Our results unify several prior findings regarding HFO mechanisms, and also make several new predictions regarding abnormal HFOs. We show that HFOs are generic, emergent phenomena whose characteristics reflect a wide range of connectivity and network input. Although produced by different mechanisms, both normal and abnormal HFOs generate similar ripple frequencies, underscoring that peak frequency is unable to distinguish the two. Abnormal ripples are generic phenomena that arise when input to pyramidal cells overcomes network inhibition, resulting in high-frequency, uncoordinated firing. In addition, fast ripples transiently and sporadically arise from the precise conditions that produce abnormal ripples. Lastly, we show that such abnormal conditions do not require any specific network structure to produce coherent HFOs, as even completely asynchronous activity is capable of producing abnormal ripples and fast ripples in this manner. These results provide a generic, network-based explanation for the link between pathological ripples and fast ripples, and a unifying description for the entire spectrum from normal ripples to pathological fast ripples."
307. Norns - Neural Network Studio (Visser & Van Gils 2014)
The Norns - Neural Network Studio is a software package for designing, simulation and analyzing networks of spiking neurons. It consists of three parts: 1. "Urd": a Matlab frontend with high-level functions for quickly defining networks 2. "Verdandi": an optimized C++ simulation environment which runs the simulation defined by Urd 3. "Skuld": an advanced Matlab graphical user interface (GUI) for visual inspection of simulated data.
308. Numerical Integration of Izhikevich and HH model neurons (Stewart and Bair 2009)
The Parker-Sochacki method is a new technique for the numerical integration of differential equations applicable to many neuronal models. Using this method, the solution order can be adapted according to the local conditions at each time step, enabling adaptive error control without changing the integration timestep. We apply the Parker-Sochacki method to the Izhikevich ‘simple’ model and a Hodgkin-Huxley type neuron, comparing the results with those obtained using the Runge-Kutta and Bulirsch-Stoer methods.
309. Olfactory bulb cluster formation (Migliore et al. 2010)
Functional roles of distributed synaptic clusters in the mitral-granule cell network of the olfactory bulb.
310. Olfactory bulb juxtaglomerular models (Carey et al., 2015)
" ...We investigated how OB circuits shape inhalation-driven dynamics in MCs using a modeling approach that was highly constrained by experimental results. First, we constructed models of canonical OB circuits that included mono- and disynaptic feedforward excitation, recurrent inhibition and feedforward inhibition of the MC. We then used experimental data to drive inputs to the models and to tune parameters; inputs were derived from sensory neuron responses during natural odorant sampling (sniffing) in awake rats, and model output was compared to recordings of MC responses to odorants sampled with the same sniff waveforms. This approach allowed us to identify OB circuit features underlying the temporal transformation of sensory inputs into inhalation-linked patterns of MC spike output. ..."
311. Olfactory bulb microcircuits model with dual-layer inhibition (Gilra & Bhalla 2015)
A detailed network model of the dual-layer dendro-dendritic inhibitory microcircuits in the rat olfactory bulb comprising compartmental mitral, granule and PG cells developed by Aditya Gilra, Upinder S. Bhalla (2015). All cell morphologies and network connections are in NeuroML v1.8.0. PG and granule cell channels and synapses are also in NeuroML v1.8.0. Mitral cell channels and synapses are in native python.
312. Olfactory bulb mitral and granule cell column formation (Migliore et al. 2007)
In the olfactory bulb, the processing units for odor discrimination are believed to involve dendrodendritic synaptic interactions between mitral and granule cells. There is increasing anatomical evidence that these cells are organized in columns, and that the columns processing a given odor are arranged in widely distributed arrays. Experimental evidence is lacking on the underlying learning mechanisms for how these columns and arrays are formed. We have used a simplified realistic circuit model to test the hypothesis that distributed connectivity can self-organize through an activity-dependent dendrodendritic synaptic mechanism. The results point to action potentials propagating in the mitral cell lateral dendrites as playing a critical role in this mechanism, and suggest a novel and robust learning mechanism for the development of distributed processing units in a cortical structure.
313. Olfactory bulb mitral and granule cell: dendrodendritic microcircuits (Migliore and Shepherd 2008)
This model shows how backpropagating action potentials in the long lateral dendrites of mitral cells, together with granule cell actions on mitral cells within narrow columns forming glomerular units, can provide a mechanism to activate strong local inhibition between arbitrarily distant mitral cells. The simulations predict a new role for the dendrodendritic synapses in the multicolumnar organization of the granule cells.
314. Olfactory bulb mitral cell gap junction NN model: burst firing and synchrony (O`Connor et al. 2012)
In a network of 6 mitral cells connected by gap junction in the apical dendrite tuft, continuous current injections of 0.06 nA are injected into 20 locations in the apical tufts of two of the mitral cells. The current injections into one of the cells starts 10 ms after the other to generate asynchronous firing in the cells (Migliore et al. 2005 protocol). Firing of the cells is asynchronous for the first 120 ms. However after the burst firing phase is completed the firing in all cells becomes synchronous.
315. Olfactory bulb mitral cell: synchronization by gap junctions (Migliore et al 2005)
In a realistic model of two electrically connected mitral cells, the paper shows that the somatically-measured experimental properties of Gap Junctions (GJs) may correspond to a variety of different local coupling strengths and dendritic distributions of GJs in the tuft. The model suggests that the propagation of the GJ-induced local tuft depolarization is a major mechanim for intraglomerular synchronization of mitral cells.
316. Olfactory Bulb mitral-granule network generates beta oscillations (Osinski & Kay 2016)
This model of the dendrodendritic mitral-granule synaptic network generates gamma and beta oscillations as a function of the granule cell excitability, which is represented by the granule cell resting membrane potential.
317. Olfactory Bulb Network (Davison et al 2003)
A biologically-detailed model of the mammalian olfactory bulb, incorporating the mitral and granule cells and the dendrodendritic synapses between them. The results of simulation experiments with electrical stimulation agree closely in most details with published experimental data. The model predicts that the time course of dendrodendritic inhibition is dependent on the network connectivity as well as on the intrinsic parameters of the synapses. In response to simulated odor stimulation, strongly activated mitral cells tend to suppress neighboring cells, the mitral cells readily synchronize their firing, and increasing the stimulus intensity increases the degree of synchronization. For more details, see the reference below.
318. Olfactory bulb network model of gamma oscillations (Bathellier et al. 2006; Lagier et al. 2007)
This model implements a network of 100 mitral cells connected with asynchronous inhibitory "synapses" that is meant to reproduce the GABAergic transmission of ensembles of connected granule cells. For appropriate parameters of this special synapse the model generates gamma oscillations with properties very similar to what is observed in olfactory bulb slices (See Bathellier et al. 2006, Lagier et al. 2007). Mitral cells are modeled as single compartment neurons with a small number of different voltage gated channels. Parameters were tuned to reproduce the fast subthreshold oscillation of the membrane potential observed experimentally (see Desmaisons et al. 1999).
319. Olfactory bulb network: neurogenetic restructuring and odor decorrelation (Chow et al. 2012)
Adult neurogenesis in the olfactory bulb has been shown experimentally to contribute to perceptual learning. Using a computational network model we show that fundamental aspects of the adult neurogenesis observed in the olfactory bulb -- the persistent addition of new inhibitory granule cells to the network, their activity-dependent survival, and the reciprocal character of their synapses with the principal mitral cells -- are sufficient to restructure the network and to alter its encoding of odor stimuli adaptively so as to reduce the correlations between the bulbar representations of similar stimuli. The model captures the experimentally observed role of neurogenesis in perceptual learning and the enhanced response of young granule cells to novel stimuli. Moreover, it makes specific predictions for the type of odor enrichment that should be effective in enhancing the ability of animals to discriminate similar odor mixtures. NSF grant DMS-0719944.
320. Olfactory Computations in Mitral-Granule cell circuits (Migliore & McTavish 2013)
Model files for the entry "Olfactory Computations in Mitral-Granule Cell Circuits" of the Springer Encyclopedia of Computational Neuroscience by Michele Migliore and Tom Mctavish. The simulations illustrate two typical Mitral-Granule cell circuits in the olfactory bulb of vertebrates: distance-independent lateral inhibition and gating effects.
321. Optimal deep brain stimulation of the subthalamic nucleus-a computational study (Feng et al. 2007)
Here, we use a biophysically-based model of spiking cells in the basal ganglia (Terman et al., Journal of Neuroscience, 22, 2963-2976, 2002; Rubin and Terman, Journal of Computational Neuroscience, 16, 211-235, 2004) to provide computational evidence that alternative temporal patterns of DBS inputs might be equally effective as the standard high-frequency waveforms, but require lower amplitudes. Within this model, DBS performance is assessed in two ways. First, we determine the extent to which DBS causes Gpi (globus pallidus pars interna) synaptic outputs, which are burstlike and synchronized in the unstimulated Parkinsonian state, to cease their pathological modulation of simulated thalamocortical cells. Second, we evaluate how DBS affects the GPi cells' auto- and cross-correlograms.
322. Orientation selectivity in inhibition-dominated recurrent networks (Sadeh and Rotter, 2015)
Emergence of contrast-invariant orientation selectivity in large-scale networks of excitatory and inhibitory neurons using integrate-and-fire neuron models.
323. Oscillating neurons in the cochlear nucleus (Bahmer Langner 2006a, b, and 2007)
"Based on the physiological and anatomical data, we propose a model consisting of a minimum network of two choppers that are interconnected with a synaptic delay of 0.4 ms (Bahmer and Langner 2006a) . Such minimum delays have been found in different systems and in various animals (e.g. Hackett, Jackson, and Rubel 1982; Borst, Helmchen, and Sakmann 1995). The choppers receive input from both the auditory nerve and an onset neuron. This model can reproduce the mean, standard deviation, and coefficient of variation of the ISI and the dynamic features of AM coding of choppers."
324. Oscillations emerging from noise-driven NNs (Tchumatchenko & Clopath 2014)
" ... Here we show how the oscillation frequency is shaped by single neuron resonance, electrical and chemical synapses.The presence of both gap junctions and subthreshold resonance are necessary for the emergence of oscillations. Our results are in agreement with several experimental observations such as network responses to oscillatory inputs and offer a much-needed conceptual link connecting a collection of disparate effects observed in networks."
325. Oscillations, phase-of-firing coding and STDP: an efficient learning scheme (Masquelier et al. 2009)
The model demonstrates how a common oscillatory drive for a group of neurons formats and reliabilizes their spike times - through an activation-to-phase conversion - so that repeating activation patterns can be easily detected and learned by a downstream neuron equipped with STDP, and then recognized in just one oscillation cycle.
326. Pallidostriatal projections promote beta oscillations (Corbit, Whalen, et al 2016)
This model consists of an inhibitory loop combining the projections from GPe neurons back to the striatum (shown experimentally to predominantly affect fast spiking interneurons, FSIs), together with the coupling from FSIs to medium spiny neurons (MSNs) in the striatum, along with the projections from MSNs to GPe. All models are in the Hodgkin-Huxley formalism, adapted from previously published models for each cell type. The connected circuit produces irregular activity under control conditions, but increasing FSI-to-MSN connectivity as observed experimentally under dopamine depletion yields exaggerated beta oscillations and synchrony. Additional mechanistic aspects are also explored.
327. Parallel network simulations with NEURON (Migliore et al 2006)
The NEURON simulation environment has been extended to support parallel network simulations. The performance of three published network models with very different spike patterns exhibits superlinear speedup on Beowulf clusters.
328. Parallel odor processing by mitral and middle tufted cells in the OB (Cavarretta et al 2016, 2018)
"[...] experimental findings suggest that MC and mTC may encode parallel and complementary odor representations. We have analyzed the functional roles of these pathways by using a morphologically and physiologically realistic three-dimensional model to explore the MC and mTC microcircuits in the glomerular layer and deeper plexiform layers. [...]"
329. Parallelizing large networks in NEURON (Lytton et al. 2016)
"Large multiscale neuronal network simulations and innovative neurotechnologies are required for development of these models requires development of new simulation technologies. We describe here the current use of the NEURON simulator with MPI (message passing interface) for simulation in the domain of moderately large networks on commonly available High Performance Computers (HPCs). We discuss the basic layout of such simulations, including the methods of simulation setup, the run-time spike passing paradigm and post-simulation data storage and data management approaches. We also compare three types of networks, ..."
330. Parametric computation and persistent gamma in a cortical model (Chambers et al. 2012)
Using the Traub et al (2005) model of the cortex we determined how 33 synaptic strength parameters control gamma oscillations. We used fractional factorial design to reduce the number of runs required to 4096. We found an expected multiplicative interaction between parameters.
331. Parvalbumin-positive basket cells differentiate among hippocampal pyramidal cells (Lee et al. 2014)
This detailed microcircuit model explores the network level effects of sublayer specific connectivity in the mouse CA1. The differences in strengths and numbers of synapses between PV+ basket cells and either superficial sublayer or deep sublayer pyramidal cells enables a routing of inhibition from superficial to deep pyramidal cells. At the network level of this model, the effects become quite prominent when one compares the effect on firing rates when either the deep or superficial pyramidal cells receive a selective increase in excitation.
332. Perceptual judgments via sensory-motor interaction assisted by cortical GABA (Hoshino et al 2018)
"Recurrent input to sensory cortex, via long-range reciprocal projections between motor and sensory cortices, is essential for accurate perceptual judgments. GABA levels in sensory cortices correlate with perceptual performance. We simulated a neuron-astrocyte network model to investigate how top-down, feedback signaling from a motor network (Nmot) to a sensory network (Nsen) affects perceptual judgments in association with ambient (extracellular) GABA levels. In the Nsen, astrocytic transporters modulated ambient GABA levels around pyramidal cells. A simple perceptual task was implemented: detection of a feature stimulus presented to the Nsen. ..."
333. Persistent synchronized bursting activity in cortical tissues (Golomb et al 2005)
The program simulates a one-dimensional model of a cortical tissue with excitatory and inhibitory populations.
334. Perturbation sensitivity implies high noise and suggests rate coding in cortex (London et al. 2010)
"... The network simulations were also based on a previously published model(Latham et al. 2000), but with modifications to allow the addition and detection of extra spikes (see Supplementary Information, section 7)."
335. Phase oscillator models for lamprey central pattern generators (Varkonyi et al. 2008)
In our paper, Varkonyi et al. 2008, we derive phase oscillator models for the lamprey central pattern generator from two biophysically based segmental models. We study intersegmental coordination and show how these models can provide stable intersegmental phase lags observed in real animals.
336. Phase precession through acceleration of local theta rhythm (Castro & Aguiar 2011)
"... Here we present a biophysical spiking model for phase precession in hippocampal CA1 which focuses on the interaction between place cells and local inhibitory interneurons. The model’s functional block is composed of a place cell (PC) connected with a local inhibitory cell (IC) which is modulated by the population theta rhythm. Both cells receive excitatory inputs from the entorhinal cortex (EC). ..."
337. Phase response theory in sparsely + strongly connected inhibitory NNs (Tikidji-Hamburyan et al 2019)
338. Phasic ACh promotes gamma oscillations in E-I networks (Lu et al, 2020)
In a biophysically-based model, we show that a network of excitatory (E) and inhibitory (I) neurons that initially displays asynchronous firing can generate transient gamma oscillatory activity in response to simulated brief pulses of ACh. ACh effects are simulated as transient modulation of the conductance of an M-type K+ current which is blocked by activation of muscarinic receptors and has significant effects on neuronal excitability. The ACh-induced effects on the M current conductance, gks, change network dynamics to promote the emergence of network gamma rhythmicity through a Pyramidal-Interneuronal Network Gamma (PING) mechanism.
339. PIR gamma oscillations in network of resonators (Tikidji-Hamburyan et al. 2015)
" ... The coupled oscillator model implemented with Wang–Buzsaki model neurons is not sufficiently robust to heterogeneity in excitatory drive, and therefore intrinsic frequency, to account for in vitro models of ING. Similarly, in a tightly synchronized regime, the stochastic population oscillator model is often characterized by sparse firing, whereas interneurons both in vivo and in vitro do not fire sparsely during gamma,but rather on average every other cycle. We substituted so-called resonator neural models, which exhibit class 2 excitability and postinhibitory rebound (PIR), for the integrators that are typically used. This results in much greater robustness to heterogeneity that actually increases as the average participation in spikes per cycle approximates physiological levels. Moreover, dynamic clamp experiments that show autapse-induced firing in entorhinal cortical interneurons support the idea that PIR can serve as a network gamma mechanism. ..."
340. Polychronization: Computation With Spikes (Izhikevich 2005)
"We present a minimal spiking network that can polychronize, that is, exhibit reproducible time-locked but not synchronous firing patterns with millisecond precision, as in synfire braids. The network consists of cortical spiking neurons with axonal conduction delays and spiketiming- dependent plasticity (STDP); a ready-to-use MATLAB code is included. It exhibits sleeplike oscillations, gamma (40 Hz) rhythms, conversion of firing rates to spike timings, and other interesting regimes. ... To our surprise, the number of coexisting polychronous groups far exceeds the number of neurons in the network, resulting in an unprecedented memory capacity of the system. ..."
341. Population models of temporal differentiation (Tripp and Eliasmith 2010)
"Temporal derivatives are computed by a wide variety of neural circuits, but the problem of performing this computation accurately has received little theoretical study. Here we systematically compare the performance of diverse networks that calculate derivatives using cell-intrinsic adaptation and synaptic depression dynamics, feedforward network dynamics, and recurrent network dynamics. Examples of each type of network are compared by quantifying the errors they introduce into the calculation and their rejection of high-frequency input noise. ..."
342. Population-level model of the basal ganglia and action selection (Gurney et al 2001, 2004)
We proposed a new functional architecture for the basal ganglia (BG) based on the premise that these brain structures play a central role in behavioural action selection. The papers quantitatively describes the properties of the model using analysis and simulation. In the first paper, we show that the decomposition of the BG into selection and control pathways is supported in several ways. First, several elegant features are exposed--capacity scaling, enhanced selectivity and synergistic dopamine modulation--which might be expected to exist in a well designed action selection mechanism. Second, good matches between model GPe output and GPi and SNr output, and neurophysiological data, have been found. Third, the behaviour of the model as a signal selection mechanism has parallels with some kinds of action selection observed in animals under various levels of dopaminergic modulation. In the second paper, we extend the BG model to include new connections, and show that action selection is maintained. In addition, we provide quantitative measures for defining different forms of selection, and methods for assessing performance changes in computational neuroscience models.
343. pre-Bötzinger complex variability (Fietkiewicz et al. 2016)
" ... Based on experimental observations, we developed a computational model that can be embedded in more comprehensive models of respiratory and cardiovascular autonomic control. Our simulation results successfully reproduce the variability we observed experimentally. The in silico model suggests that age-dependent variability may be due to a developmental increase in mean synaptic conductance between preBötC neurons. We also used simulations to explore the effects of stochastic spiking in sensory relay neurons. Our results suggest that stochastic spiking may actually stabilize modulation of both respiratory rate and its variability when the rate changes due to physiological demand. "
344. Principles of Computational Modelling in Neuroscience (Book) (Sterratt et al. 2011)
"... This book provides a step-by-step account of how to model the neuron and neural circuitry to understand the nervous system at all levels, from ion channels to networks. Starting with a simple model of the neuron as an electrical circuit, gradually more details are added to include the effects of neuronal morphology, synapses, ion channels and intracellular signaling. The principle of abstraction is explained through chapters on simplifying models, and how simplified models can be used in networks. This theme is continued in a final chapter on modeling the development of the nervous system. Requiring an elementary background in neuroscience and some high school mathematics, this textbook is an ideal basis for a course on computational neuroscience."
345. Prosthetic electrostimulation for information flow repair in a neocortical simulation (Kerr 2012)
This model is an extension of a model (<a href="http://senselab.med.yale.edu/ModelDB/ShowModel.asp?model=138379">138379</a>) recently published in Frontiers in Computational Neuroscience. This model consists of 4700 event-driven, rule-based neurons, wired according to anatomical data, and driven by both white-noise synaptic inputs and a sensory signal recorded from a rat thalamus. Its purpose is to explore the effects of cortical damage, along with the repair of this damage via a neuroprosthesis.
346. Purkinje cell: Synaptic activation predicts voltage control of burst-pause (Masoli & D'Angelo 2017)
"The dendritic processing in cerebellar Purkinje cells (PCs), which integrate synaptic inputs coming from hundreds of thousands granule cells and molecular layer interneurons, is still unclear. Here we have tested a leading hypothesis maintaining that the significant PC output code is represented by burst-pause responses (BPRs), by simulating PC responses in a biophysically detailed model that allowed to systematically explore a broad range of input patterns. BPRs were generated by input bursts and were more prominent in Zebrin positive than Zebrin negative (Z+ and Z-) PCs. Different combinations of parallel fiber and molecular layer interneuron synapses explained type I, II and III responses observed in vivo. BPRs were generated intrinsically by Ca-dependent K channel activation in the somato-dendritic compartment and the pause was reinforced by molecular layer interneuron inhibition. BPRs faithfully reported the duration and intensity of synaptic inputs, such that synaptic conductance tuned the number of spikes and release probability tuned their regularity in the millisecond range. ..."
347. Purkinje neuron network (Zang et al. 2020)
Both spike rate and timing can transmit information in the brain. Phase response curves (PRCs) quantify how a neuron transforms input to output by spike timing. PRCs exhibit strong firing-rate adaptation, but its mechanism and relevance for network output are poorly understood. Using our Purkinje cell (PC) model we demonstrate that the rate adaptation is caused by rate-dependent subthreshold membrane potentials efficiently regulating the activation of Na+ channels. Then we use a realistic PC network model to examine how rate-dependent responses synchronize spikes in the scenario of reciprocal inhibition-caused high-frequency oscillations. The changes in PRC cause oscillations and spike correlations only at high firing rates. The causal role of the PRC is confirmed using a simpler coupled oscillator network model. This mechanism enables transient oscillations between fast-spiking neurons that thereby form PC assemblies. Our work demonstrates that rate adaptation of PRCs can spatio-temporally organize the PC input to cerebellar nuclei.
348. Pyramidal neuron, fast, regular, and irregular spiking interneurons (Konstantoudaki et al 2014)
This is a model network of prefrontal cortical microcircuit based primarily on rodent data. It includes 16 pyramidal model neurons, 2 fast spiking interneuron models, 1 regular spiking interneuron model and 1 irregular spiking interneuron model. The goal of the paper was to use this model network to determine the role of specific interneuron subtypes in persistent activity
349. Quantitative assessment of computational models for retinotopic map formation (Hjorth et al. 2015)
"Molecular and activity-based cues acting together are thought to guide retinal axons to their terminal sites in vertebrate optic tectum or superior colliculus (SC) to form an ordered map of connections. The details of mechanisms involved, and the degree to which they might interact, are still not well understood. We have developed a framework within which existing computational models can be assessed in an unbiased and quantitative manner against a set of experimental data curated from the mouse retinocollicular system. ..."
350. Rapid desynchronization of an electrically coupled Golgi cell network (Vervaeke et al. 2010)
Electrical synapses between interneurons contribute to synchronized firing and network oscillations in the brain. However, little is known about how such networks respond to excitatory synaptic input. In addition to detailed electrophysiological recordings and histological investigations of electrically coupled Golgi cells in the cerebellum, a detailed network model of these cells was created. The cell models are based on reconstructed Golgi cell morphologies and the active conductances are taken from an earlier abstract Golgi cell model (Solinas et al 2007, accession no. 112685). Our results show that gap junction coupling can sometimes be inhibitory and either promote network synchronization or trigger rapid network desynchronization depending on the synaptic input. The model is available as a neuroConstruct project and can executable scripts can be generated for the NEURON simulator.
351. Rate model of a cortical RS-FS-LTS network (Hayut et al. 2011)
A rate model of cortical networks composed of RS, FS and LTS neurons. Synaptic depression is modelled according to the Tsodyks-Markram scheme.
352. Reconstrucing sleep dynamics with data assimilation (Sedigh-Sarvestani et al., 2012)
We have developed a framework, based on the unscented Kalman filter, for estimating hidden states and parameters of a network model of sleep. The network model includes firing rates and neurotransmitter output of 5 cell-groups in the rat brain.
353. Recurrent amplification of grid-cell activity (D'Albis and Kempter 2020)
354. Reducing variability in motor cortex activity by GABA (Hoshino et al. 2019)
Interaction between sensory and motor cortices is crucial for perceptual decision-making, in which intracortical inhibition might have an important role. We simulated a neural network model consisting of a sensory network (NS) and a motor network (NM) to elucidate the significance of their interaction in perceptual decision-making in association with the level of GABA in extracellular space: extracellular GABA concentration. Extracellular GABA molecules acted on extrasynaptic receptors embedded in membranes of pyramidal cells and suppressed them. A reduction in extracellular GABA concentration either in NS or NM increased the rate of errors in perceptual decision-making, for which an increase in ongoing-spontaneous fluctuations in subthreshold neuronal activity in NM prior to sensory stimulation was responsible. Feedback (NM-to-NS) signaling enhanced selective neuronal responses in NS, which in turn increased stimulus-evoked neuronal activity in NM. We suggest that GABA in extracellular space contributes to reducing variability in motor cortex activity at a resting state and thereby the motor cortex can respond correctly to a subsequent sensory stimulus. Feedback signaling from the motor cortex improves the selective responsiveness of the sensory cortex, which ensures the fidelity of information transmission to the motor cortex, leading to reliable perceptual decision-making.
355. Regulation of a slow STG rhythm (Nadim et al 1998)
Frequency regulation of a slow rhythm by a fast periodic input. Nadim, F., Manor, Y., Nusbaum, M. P., Marder, E. (1998) J. Neurosci. 18: 5053-5067
356. Reichardt Model for Motion Detection in the Fly Visual System (Tuthill et al, 2011)
This simulation implements a correlation-type model for visual motion detection, as originally described by Hassenstein and Reichardt (1956), and analyzes the response of the model to standard and reverse-phi motion stimuli. Details are provided in: Tuthill JC, et al. (2011)
357. Reinforcement learning of targeted movement (Chadderdon et al. 2012)
"Sensorimotor control has traditionally been considered from a control theory perspective, without relation to neurobiology. In contrast, here we utilized a spiking-neuron model of motor cortex and trained it to perform a simple movement task, which consisted of rotating a single-joint “forearm” to a target. Learning was based on a reinforcement mechanism analogous to that of the dopamine system. This provided a global reward or punishment signal in response to decreasing or increasing distance from hand to target, respectively. Output was partially driven by Poisson motor babbling, creating stochastic movements that could then be shaped by learning. The virtual forearm consisted of a single segment rotated around an elbow joint, controlled by flexor and extensor muscles. ..."
358. Relative spike time coding and STDP-based orientation selectivity in V1 (Masquelier 2012)
Phenomenological spiking model of the cat early visual system. We show how natural vision can drive spike time correlations on sufficiently fast time scales to lead to the acquisition of orientation-selective V1 neurons through STDP. This is possible without reference times such as stimulus onsets, or saccade landing times. But even when such reference times are available, we demonstrate that the relative spike times encode the images more robustly than the absolute ones.
359. Respiratory central pattern generator including Kolliker-Fuse nucleus (Wittman et al 2019)
We present three highly reduced conductance-based models for the core of the respiratory CPG. All successfully simulate respiratory outputs across eupnoeic and vagotomized conditions and show that loss of inhibition to the pontine Kolliker-Fuse nucleus reproduces the key respiratory alterations associated with Rett syndrome.
360. Respiratory central pattern generator network in mammalian brainstem (Rubin et al. 2009)
This model is a reduced version of a spatially organized respiratory central pattern generation network consisting of four neuronal populations (pre-I, early-I, post-I, and aug-E). In this reduction, each population is represented by a single neuron, in an activity-based framework (which includes the persistent sodium current for the pre-I population). The model includes three sources of external drive and can produce several experimentally observed rhythms.
361. Response properties of neocort. neurons to temporally modulated noisy inputs (Koendgen et al. 2008)
Neocortical neurons are classified by current–frequency relationship. This is a static description and it may be inadequate to interpret neuronal responses to time-varying stimuli. Theoretical studies (Brunel et al., 2001; Fourcaud-Trocmé et al. 2003; Fourcaud-Trocmé and Brunel 2005; Naundorf et al. 2005) suggested that single-cell dynamical response properties are necessary to interpret ensemble responses to fast input transients. Further, it was shown that input-noise linearizes and boosts the response bandwidth, and that the interplay between the barrage of noisy synaptic currents and the spike-initiation mechanisms determine the dynamical properties of the firing rate. In order to allow a reader to explore such simulations, we prepared a simple NEURON implementation of the experiments performed in Köndgen et al., 2008 (see also Fourcaud-Trocmé al. 2003; Fourcaud-Trocmé and Brunel 2005). In addition, we provide sample MATLAB routines for exploring the sandwich model proposed in Köndgen et al., 2008, employing a simple frequdency-domain filtering. The simulations and the MATLAB routines are based on the linear response properties of layer 5 pyramidal cells estimated by injecting a superposition of a small-amplitude sinusoidal wave and a background noise, as in Köndgen et al., 2008.
362. Reverberatory bursts propagation and synchronization in developing cultured NNs (Huang et al 2016)
"Developing networks of neural systems can exhibit spontaneous, synchronous activities called neural bursts, which can be important in the organization of functional neural circuits. ... Using a propagation model we infer the spreading speed of the spiking activity, which increases as the culture ages. We perform computer simulations of the system using a physiological model of spiking networks in two spatial dimensions and find the parameters that reproduce the observed resynchronization of spiking in the bursts. An analysis of the simulated dynamics suggests that the depletion of synaptic resources causes the resynchronization. The spatial propagation dynamics of the simulations match well with observations over the course of a burst and point to an interplay of the synaptic efficacy and the noisy neural self-activation in producing the morphology of the bursts."
363. Reward modulated STDP (Legenstein et al. 2008)
"... This article provides tools for an analytic treatment of reward-modulated STDP, which allows us to predict under which conditions reward-modulated STDP will achieve a desired learning effect. These analytical results imply that neurons can learn through reward-modulated STDP to classify not only spatial but also temporal firing patterns of presynaptic neurons. They also can learn to respond to specific presynaptic firing patterns with particular spike patterns. Finally, the resulting learning theory predicts that even difficult credit-assignment problems, where it is very hard to tell which synaptic weights should be modified in order to increase the global reward for the system, can be solved in a self-organizing manner through reward-modulated STDP. This yields an explanation for a fundamental experimental result on biofeedback in monkeys by Fetz and Baker. In this experiment monkeys were rewarded for increasing the firing rate of a particular neuron in the cortex and were able to solve this extremely difficult credit assignment problem. ... In addition our model demonstrates that reward-modulated STDP can be applied to all synapses in a large recurrent neural network without endangering the stability of the network dynamics."
364. Robust Reservoir Generation by Correlation-Based Learning (Yamazaki & Tanaka 2008)
"Reservoir computing (RC) is a new framework for neural computation. A reservoir is usually a recurrent neural network with fixed random connections. In this article, we propose an RC model in which the connections in the reservoir are modifiable. ... We apply our RC model to trace eyeblink conditioning. The reservoir bridged the gap of an interstimulus interval between the conditioned and unconditioned stimuli, and a readout neuron was able to learn and express the timed conditioned response."
365. Role for short term plasticity and OLM cells in containing spread of excitation (Hummos et al 2014)
This hippocampus model was developed by matching experimental data, including neuronal behavior, synaptic current dynamics, network spatial connectivity patterns, and short-term synaptic plasticity. Furthermore, it was constrained to perform pattern completion and separation under the effects of acetylcholine. The model was then used to investigate the role of short-term synaptic depression at the recurrent synapses in CA3, and inhibition by basket cell (BC) interneurons and oriens lacunosum-moleculare (OLM) interneurons in containing the unstable spread of excitatory activity in the network.
366. S cell network (Moss et al 2005)
Excerpts from the abstract: S cells form a chain of electrically coupled neurons that extends the length of the leech CNS and plays a critical role in sensitization during whole-body shortening. ... Serotonin ... increasedAP latency across the electrical synapse, suggesting that serotonin reduced coupling between S cells. ... Serotonin modulated instantaneous AP frequency when APs were initiated in separate S cells and in a computational model of S cell activity following mechanosensory input. Thus, serotonergic modulation of S cell electrical synapses may contribute to changes in the pattern of activity in the S cell network. See paper for more.
367. SCN1A gain-of-function in early infantile encephalopathy (Berecki et al 2019)
"OBJECTIVE: To elucidate the biophysical basis underlying the distinct and severe clinical presentation in patients with the recurrent missense SCN1A variant, p.Thr226Met. Patients with this variant show a well-defined genotype-phenotype correlation and present with developmental and early infantile epileptic encephalopathy that is far more severe than typical SCN1A Dravet syndrome. METHODS: Whole cell patch clamp and dynamic action potential clamp were used to study T226M Nav 1.1 channels expressed in mammalian cells. Computational modeling was used to explore the neuronal scale mechanisms that account for altered action potential firing. RESULTS: T226M channels exhibited hyperpolarizing shifts of the activation and inactivation curves and enhanced fast inactivation. Dynamic action potential clamp hybrid simulation showed that model neurons containing T226M conductance displayed a left shift in rheobase relative to control. At current stimulation levels that produced repetitive action potential firing in control model neurons, depolarization block and cessation of action potential firing occurred in T226M model neurons. Fully computationally simulated neuron models recapitulated the findings from dynamic action potential clamp and showed that heterozygous T226M models were also more susceptible to depolarization block. ..."
368. Self-organized olfactory pattern recognition (Kaplan & Lansner 2014)
" ... We present a large-scale network model with single and multi-compartmental Hodgkin–Huxley type model neurons representing olfactory receptor neurons (ORNs) in the epithelium, periglomerular cells, mitral/tufted cells and granule cells in the olfactory bulb (OB), and three types of cortical cells in the piriform cortex (PC). Odor patterns are calculated based on affinities between ORNs and odor stimuli derived from physico-chemical descriptors of behaviorally relevant real-world odorants. ... The PC was implemented as a modular attractor network with a recurrent connectivity that was likewise organized through Hebbian–Bayesian learning. We demonstrate the functionality of the model in a one-sniff-learning and recognition task on a set of 50 odorants. Furthermore, we study its robustness against noise on the receptor level and its ability to perform concentration invariant odor recognition. Moreover, we investigate the pattern completion capabilities of the system and rivalry dynamics for odor mixtures."
369. Sensitivity of noisy neurons to coincident inputs (Rossant et al. 2011)
"Two distant or coincident spikes are injected into a noisy balanced leaky integrate-and-fire neuron. The PSTH of the neuron in response to these inputs is calculated along with the extra number of spikes in the two cases. This number is higher for the coincident spikes, showing the sensitivity of a noisy neuron to coincident inputs."
370. Sensorimotor cortex reinforcement learning of 2-joint virtual arm reaching (Neymotin et al. 2013)
"... We developed a model of sensory and motor neocortex consisting of 704 spiking model-neurons. Sensory and motor populations included excitatory cells and two types of interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a 2-joint virtual arm to reach to a fixed target. ... "
371. Sensory feedback in an oscillatory interference model of place cell activity (Monaco et al. 2011)
Many animals use a form of dead reckoning known as 'path integration' to maintain a sense of their location as they explore the world. However, internal motion signals and the neural activity that integrates them can be noisy, leading inevitably to inaccurate position estimates. The rat hippocampus and entorhinal cortex support a flexible system of spatial representation that is critical to spatial learning and memory. The position signal encoded by this system is thought to rely on path integration, but it must be recalibrated by familiar landmarks to maintain accuracy. To explore the interaction between path integration and external landmarks, we present a model of hippocampal activity based on the interference of theta-frequency oscillations that are modulated by realistic animal movements around a track. We show that spatial activity degrades with noise, but introducing external cues based on direct sensory feedback can prevent this degradation. When these cues are put into conflict with each other, their interaction produces a diverse array of response changes that resembles experimental observations. Feedback driven by attending to landmarks may be critical to navigation and spatial memory in mammals.
372. Sensory-evoked responses of L5 pyramidal tract neurons (Egger et al 2020)
This is the L5 pyramidal tract neuron (L5PT) model from Egger, Narayanan et al., Neuron 2020. It allows investigating how synaptic inputs evoked by different sensory stimuli are integrated by the complex intrinsic properties of L5PTs. The model is constrained by anatomical measurements of the subcellular synaptic input patterns to L5PT neurons, in vivo measurements of sensory-evoked responses of different populations of neurons providing these synaptic inputs, and in vitro measurements constraining the biophysical properties of the soma, dendrites and axon (note: the biophysical model is based on the work by Hay et al., Plos Comp Biol 2011). The model files provided here allow performing simulations and analyses presented in Figures 3, 4 and 5.
373. Simulated cortical color opponent receptive fields self-organize via STDP (Eguchi et al., 2014)
"... In this work, we address the problem of understanding the cortical processing of color information with a possible mechanism of the development of the patchy distribution of color selectivity via computational modeling. ... Our model of the early visual system consists of multiple topographically-arranged layers of excitatory and inhibitory neurons, with sparse intra-layer connectivity and feed-forward connectivity between layers. Layers are arranged based on anatomy of early visual pathways, and include a retina, lateral geniculate nucleus, and layered neocortex. ... After training with natural images, the neurons display heightened sensitivity to specific colors. ..."
374. Simulation studies on mechanisms of levetiracetam-mediated inhibition of IK(DR) (Huang et al. 2009)
Levetiracetam (LEV) is an S-enantiomer pyrrolidone derivative with established antiepileptic efficacy in generalized epilepsy and partial epilepsy. However, its effects on ion currents and membrane potential remain largely unclear. In this study, we investigated the effect of LEV on differentiated NG108-15 neurons. ... Simulation studies in a modified Hodgkin-Huxley neuron and network unraveled that the reduction of slowly inactivating IK(DR) resulted in membrane depolarization accompanied by termination of the firing of action potentials in a stochastic manner. Therefore, the inhibitory effects on slowly inactivating IK(DR) (Kv3.1-encoded current) may constitute one of the underlying mechanisms through which LEV affects neuronal activity in vivo.
375. Simulation system of spinal cord motor nuclei and assoc. nerves and muscles (Cisi and Kohn 2008)
A Web-based simulation system of the spinal cord circuitry responsible for muscle control is described. The simulator employs two-compartment motoneuron models for S, FR and FF types, with synaptic inputs acting through conductance variations. Four motoneuron pools with their associated interneurons are represented in the simulator, with the possibility of inclusion of more than 2,000 neurons and 2,000,000 synapses. ... Inputs to the motoneuron pool come from populations of interneurons (Ia reciprocal inhibitory interneurons, Ib interneurons, and Renshaw cells) and from stochastic point processes associated with descending tracts. ... The generation of the H-reflex by the Ia-motoneuron pool system and its modulation by spinal cord interneurons is included in the simulation system.
376. Simulations of oscillations in piriform cortex (Wilson & Bower 1992)
"1. A large-scale computer model of the piriform cortex was constructed on the basis of the known anatomic and physiological organization of this region. 2. The oscillatory field potential and electroencephalographic (EEG) activity generated by the model was compared with actual physiological results. The model was able to produce patterns of activity similar to those recorded physiologically in response to both weak and strong electrical shocks to the afferent input. The model also generated activity patterns similar to EEGs recorded in behaving animals. 3. ..."
377. Single E-I oscillating network with amplitude modulation (Avella Gonzalez et al. 2012)
"... Intriguingly, the amplitude of ongoing oscillations, such as measured in EEG recordings, fluctuates irregularly, with episodes of high amplitude (HAE) alternating with episodes of low amplitude (LAE). ... Here, we show that transitions between HAE and LAE in the alpha/beta frequency band occur in a generic neuronal network model consisting of interconnected inhibitory (I) and excitatory (E) cells that are externally driven by sustained depolarizing currents(cholinergic input) and trains of action potentials that activate excitatory synapses. In the model, action potentials onto inhibitory cells represent input from other brain areas and desynchronize network activity, being crucial for the emergence of amplitude fluctuations. ..."
378. Single Trial Sequence learning: a spiking neurons model based on hippocampus (Coppolino et al 2021)
In contrast with our everyday experience using brain circuits, it can take a prohibitively long time to train a computational system to produce the correct sequence of outputs in the presence of a series of inputs. This suggests that something important is missing in the way in which models are trying to reproduce basic cognitive functions. In this work, we introduce a new neuronal network architecture that is able to learn, in a single trial, an arbitrary long sequence of any known objects. The key point of the model is the explicit use of mechanisms and circuitry observed in the hippocampus. By directly following the natural system’s layout and circuitry, this type of implementation has the additional advantage that the results can be more easily compared to experimental data, allowing a deeper and more direct understanding of the mechanisms underlying cognitive functions and dysfunctions.
379. Sleep-wake transitions in corticothalamic system (Bazhenov et al 2002)
The authors investigate the transition between sleep and awake states with intracellular recordings in cats and computational models. The model describes many essential features of slow wave sleep and activated states as well as the transition between them.
380. Slow wave propagation in the guinea-pig gastric antrum (Hirst et al. 2006, Edwards and Hirst 2006)
"(Edwards and Hirst 2006) provides an electrical description of the propagation of slow waves and pacemaker potentials in the guinea-pig gastric antrum in anal and circumferential directions. As electrical conduction between laterally adjacent circular muscle bundles is regularly interrupted, anal conduction of pacemaker potentials was assumed to occur via an electrically interconnected chain of myenteric interstitial cells of Cajal (ICCMY). ICCMY were also connected resistively to serially connected compartments of longitudinal muscle. Circumferential conduction occurred in a circular smooth muscle bundle that was represented as a chain of electrically connected isopotential compartments: each compartment contained a proportion of intramuscular interstitial cells of Cajal (ICCIM) that are responsible for the regenerative component of the slow wave. The circular muscle layer, which contains ICCIM, and the ICCMY network incorporated a mechanism, modelled as a two-stage chemical reaction, which produces an intracellular messenger. ... The model generates pacemaker potentials and slow waves with propagation velocities similar to those determined in the physiological experiments described in the accompanying paper."
381. Small world networks of Type I and Type II Excitable Neurons (Bogaard et al. 2009)
Implemented with NEURON 5.9, four model neurons with varying excitability properties affect the spatiotemporal patterning of small world networks of homogeneous and heterogeneous cell population.
382. Software for teaching neurophysiology of neuronal circuits (Grisham et al. 2008)
"To circumvent the many problems in teaching neurophysiology as a “wet lab,” we developed SWIMMY, a virtual fish that swims by moving its virtual tail by means of a virtual neural circuit. ... Using SWIMMY, students (1) review the basics of neurophysiology, (2) identify the neurons in the circuit, (3) ascertain the neurons’ synaptic interconnections, (4) discover which cells generate the motor pattern of swimming, (5) discover how the rhythm is generated, and finally (6) use an animation that corresponds to the activity of the motoneurons to discover the behavioral effects produced by various lesions and explain them in terms of their neural underpinnings. ..."
383. Sparse connectivity is required for decorrelation, pattern separation (Cayco-Gajic et al 2017)
" ... To investigate the structural and functional determinants of pattern separation we built models of the cerebellar input layer with spatially correlated input patterns, and systematically varied their synaptic connectivity. ..."
384. Spike burst-pause dynamics of Purkinje cells regulate sensorimotor adaptation (Luque et al 2019)
"Cerebellar Purkinje cells mediate accurate eye movement coordination. However, it remains unclear how oculomotor adaptation depends on the interplay between the characteristic Purkinje cell response patterns, namely tonic, bursting, and spike pauses. Here, a spiking cerebellar model assesses the role of Purkinje cell firing patterns in vestibular ocular reflex (VOR) adaptation. The model captures the cerebellar microcircuit properties and it incorporates spike-based synaptic plasticity at multiple cerebellar sites. ..."
385. Spike exchange methods for a Blue Gene/P supercomputer (Hines et al., 2011)
Tests several spike exchange methods on a Blue Gene/P supercomputer on up to 64K cores.
386. Spike-Timing-Based Computation in Sound Localization (Goodman and Brette 2010)
" ... In neuron models consisting of spectro-temporal filtering and spiking nonlinearity, we found that the binaural structure induced by spatialized sounds is mapped to synchrony patterns that depend on source location rather than on source signal. Location-specific synchrony patterns would then result in the activation of location-specific assemblies of postsynaptic neurons. We designed a spiking neuron model which exploited this principle to locate a variety of sound sources in a virtual acoustic environment using measured human head-related transfer functions. ..."
387. Spikes,synchrony,and attentive learning by laminar thalamocort. circuits (Grossberg & Versace 2007)
"... The model hereby clarifies, for the first time, how the following levels of brain organization coexist to realize cognitive processing properties that regulate fast learning and stable memory of brain representations: single cell properties, such as spiking dynamics, spike-timing-dependent plasticity (STDP), and acetylcholine modulation; detailed laminar thalamic and cortical circuit designs and their interactions; aggregate cell recordings, such as current-source densities and local field potentials; and single cell and large-scale inter-areal oscillations in the gamma and beta frequency domains. ..."
388. Spiking GridPlaceMap model (Pilly & Grossberg, PLoS One, 2013)
Development of spiking grid cells and place cells in the entorhinal-hippocampal system to represent positions in large spaces
389. Spiking neuron model of the basal ganglia (Humphries et al 2006)
A spiking neuron model of the basal ganglia (BG) circuit (striatum, STN, GP, SNr). Includes: parallel anatomical channels; tonic dopamine; dopamine receptors in striatum, STN, and GP; burst-firing in STN; GABAa, AMPA, and NMDA currents; effects of synaptic location. Model demonstrates selection and switching of input signals. Replicates experimental data on changes in slow-wave (<1 Hz) and gamma-band oscillations within BG nuclei following lesions and pharmacological manipulations.
390. Spinal circuits controlling limb coordination and gaits in quadrupeds (Danner et al 2017)
Simulation of spinal neural networks involved in the central control of interlimb coordination and speed-dependent gait expression in quadrupeds.
391. Spontaneous weakly correlated excitation and inhibition (Tan et al. 2013)
Brian code for Tan et al. 2013.
392. Stability of complex spike timing-dependent plasticity in cerebellar learning (Roberts 2007)
"Dynamics of spike-timing dependent synaptic plasticity are analyzed for excitatory and inhibitory synapses onto cerebellar Purkinje cells. The purpose of this study is to place theoretical constraints on candidate synaptic learning rules that determine the changes in synaptic efficacy due to pairing complex spikes with presynaptic spikes in parallel fibers and inhibitory interneurons. ..."
393. Stable propagation of synchronous spiking in cortical neural networks (Diesmann et al 1999)
"... Here we show that precisely synchronized action potentials can propagate within a model of cortical network activity that recapitulates many of the features of biological systems. An attractor, yielding a stable spiking precision in the (sub)millisecond range, governs the dynamics of synchronization. Our results indicate that a combinatorial neural code, based on rapid associations of groups of neurons co-ordinating their activity at the single spike level, is possible within a cortical-like network."
394. State dependent drug binding to sodium channels in the dentate gyrus (Thomas & Petrou 2013)
A Markov model of sodium channels was developed that includes drug binding to fast inactivated states. This was incorporated into a model of the dentate gyrus to investigate the effects of anti-epileptic drugs on neuron and network properties.
395. State-dependent rhythmogenesis in a half-center locomotor CPG (Ausborn et al 2017)
"The spinal locomotor central pattern generator (CPG) generates rhythmic activity with alternating flexion and extension phases. This rhythmic pattern is likely to result from inhibitory interactions between neural populations representing flexor and extensor half-centers. However, it is unclear whether the flexor-extensor CPG has a quasi-symmetric organization with both half-centers critically involved in rhythm generation, features an asymmetric organization with flexor-driven rhythmogenesis, or comprises a pair of intrinsically rhythmic half-centers. There are experimental data that support each of the above concepts but appear to be inconsistent with the others. In this theoretical/modeling study, we present and analyze a CPG model architecture that can operate in different regimes consistent with the above three concepts depending on conditions, which are defined by external excitatory drives to CPG half-centers. We show that control of frequency and phase durations within each regime depends on network dynamics, defined by the regime-dependent expression of the half-centers' intrinsic rhythmic capabilities and the operating phase transition mechanisms (escape vs. release). Our study suggests state dependency in locomotor CPG operation and proposes explanations for seemingly contradictory experimental data."
396. Statistics of symmetry measure for networks of neurons (Esposito et al. 2014)
The code reproduces Figures 1, 2, 3A and 3C from Esposito et al "Measuring symmetry, asymmetry and randomness in neural networks". It provides the statistics of the symmetry measure defined in the paper for networks of neurons with random connections drawn from uniform and gaussian distributions.
397. Status epilepticus alters dentate basket cell tonic inhibition (Yu J et al 2013)
Status epilepticus (SE) leads to changes in dentate inhibitory neuronal networks and alters synaptic and tonic inhibition in granule cells. Recently, we identified that one week after pilocarpine-induced status epilepticus, dentate fast-spiking basket cells (FS-BCs), which underlie fast perisomatic inhibition, show two distinct changes in inhibition: (1) enhanced tonic currents (IGABA) and (2)depolarizing shift in GABA reversal (EGABA) following SE. These two changes can have opposing effects on neuronal inhibition with increases in tonic GABA conductance (gGABA) reducing excitability when the GABA currents are shunting (or hyperpolarizing) and potentially enhancing excitability when GABA currents are depolarizing. The following model is used to examine the post-SE changes in tonic GABA conductance, together with the depolarized GABA reversal potential modify FS-BC excitability and dentate network activity.
398. STDP allows fast rate-modulated coding with Poisson-like spike trains (Gilson et al. 2011)
The model demonstrates that a neuron equipped with STDP robustly detects repeating rate patterns among its afferents, from which the spikes are generated on the fly using inhomogenous Poisson sampling, provided those rates have narrow temporal peaks (10-20ms) - a condition met by many experimental Post-Stimulus Time Histograms (PSTH).
399. STDP promotes synchrony of inhibitory networks in the presence of heterogeneity (Talathi et al 2008)
"Recently Haas et al. (J Neurophysiol 96: 3305–3313, 2006), observed a novel form of spike timing dependent plasticity (iSTDP) in GABAergic synaptic couplings in layer II of the entorhinal cortex. Depending on the relative timings of the presynaptic input at time tpre and the postsynaptic excitation at time tpost, the synapse is strengthened (delta_t = t(post) - t(pre) > 0) or weakened (delta_t < 0). The temporal dynamic range of the observed STDP rule was found to lie in the higher gamma frequency band (> or = 40 Hz), a frequency range important for several vital neuronal tasks. In this paper we study the function of this novel form of iSTDP in the synchronization of the inhibitory neuronal network. In particular we consider a network of two unidirectionally coupled interneurons (UCI) and two mutually coupled interneurons (MCI), in the presence of heterogeneity in the intrinsic firing rates of each coupled neuron. ..."
400. Stochastic and periodic inputs tune ongoing oscillations (Hutt et al. 2016)
" ... We here analyze a network of recurrently connected spiking neurons with time delay displaying stable synchronous dynamics. Using mean-field and stability analyses, we investigate the influence of dynamic inputs on the frequency of firing rate oscillations. ..."
401. Storing serial order in intrinsic excitability: a working memory model (Conde-Sousa & Aguiar 2013)
" … Here we present a model for working memory which relies on the modulation of the intrinsic excitability properties of neurons, instead of synaptic plasticity, to retain novel information for periods of seconds to minutes. We show that it is possible to effectively use this mechanism to store the serial order in a sequence of patterns of activity. … The presented model exhibits properties which are in close agreement with experimental results in working memory. ... "
402. Striatal dopamine ramping: an explanation by reinforcement learning with decay (Morita & Kato, 2014)
Incorporation of decay of learned values into temporal-difference (TD) learning (Sutton & Barto, 1998, Reinforcement Learning (MIT Press)) causes ramping of TD reward prediction error (RPE), which could explain, given the hypothesis that dopamine represents TD RPE (Montague et al., 1996, J Neurosci 16:1936; Schultz et al., 1997, Science 275:1593), the reported ramping of the dopamine concentration in the striatum in a reward-associated spatial navigation task (Howe et al., 2013, Nature 500:575).
403. Striatal GABAergic microcircuit, dopamine-modulated cell assemblies (Humphries et al. 2009)
To begin identifying potential dynamically-defined computational elements within the striatum, we constructed a new three-dimensional model of the striatal microcircuit's connectivity, and instantiated this with our dopamine-modulated neuron models of the MSNs and FSIs. A new model of gap junctions between the FSIs was introduced and tuned to experimental data. We introduced a novel multiple spike-train analysis method, and apply this to the outputs of the model to find groups of synchronised neurons at multiple time-scales. We found that, with realistic in vivo background input, small assemblies of synchronised MSNs spontaneously appeared, consistent with experimental observations, and that the number of assemblies and the time-scale of synchronisation was strongly dependent on the simulated concentration of dopamine. We also showed that feed-forward inhibition from the FSIs counter-intuitively increases the firing rate of the MSNs.
404. Striatal GABAergic microcircuit, spatial scales of dynamics (Humphries et al, 2010)
The main thrust of this paper was the development of the 3D anatomical network of the striatum's GABAergic microcircuit. We grew dendrite and axon models for the MSNs and FSIs and extracted probabilities for the presence of these neurites as a function of distance from the soma. From these, we found the probabilities of intersection between the neurites of two neurons given their inter-somatic distance, and used these to construct three-dimensional striatal networks. These networks were examined for their predictions for the distributions of the numbers and distances of connections for all the connections in the microcircuit. We then combined the neuron models from a previous model (Humphries et al, 2009; ModelDB ID: 128874) with the new anatomical model. We used this new complete striatal model to examine the impact of the anatomical network on the firing properties of the MSN and FSI populations, and to study the influence of all the inputs to one MSN within the network.
405. Striatal NN model of MSNs and FSIs investigated effects of dopamine depletion (Damodaran et al 2015)
This study investigates the mechanisms that are affected in the striatal network after dopamine depletion and identifies potential therapeutic targets to restore normal activity.
406. Structure-dynamics relationships in bursting neuronal networks revealed (Mäki-Marttunen et al. 2013)
This entry includes tools for generating and analyzing network structure, and for running the neuronal network simulations on them.
407. Studies of stimulus parameters for seizure disruption using NN simulations (Anderson et al. 2007)
Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. Wiring is adapted to minicolumn hypothesis and incorporates visual and neocortical data. Simulation demonstrates spontaneous bursting onset and cessation, and activity can be altered with external electric field.
408. Study of augmented Rubin and Terman 2004 deep brain stim. model in Parkinsons (Pascual et al. 2006)
" ... The model by Rubin and Terman [31] represents one of the most comprehensive and biologically plausible models of DBS published recently. We examined the validity of the model, replicated its simulations and tested its robustness. While our simulations partially reproduced the results presented by Rubin and Terman [31], several issues were raised including the high complexity of the model in its non simplified form, the lack of robustness of the model with respect to small perturbations, the nonrealistic representation of the thalamus and the absence of time delays. Computational models are indeed necessary, but they may not be sufficient in their current forms to explain the effect of chronic electrical stimulation on the activity of the basal ganglia (BG) network in PD."
409. Subiculum network model with dynamic chloride/potassium homeostasis (Buchin et al 2016)
This is the code implementing the single neuron and spiking neural network dynamics. The network has the dynamic ion concentrations of extracellular potassium and intracellular chloride. The code contains multiple parameter variations to study various mechanisms of the neural excitability in the context of chloride homeostasis.
410. Surround Suppression in V1 via Withdraw of Balanced Local Excitation in V1 (Shushruth 2012)
The model is mean-field network models, which is set up as a so-called ring-model, i. e. it is a highly idealized model of an orientation hypercolumn in primary visual cortex. Long-range intra-areal and inter-areal feedback connections are modeled phenomenologically as an external input. In this model, there are recurrent interactions via short-range local connections between orientation columns, but not between hypercolumns.
411. Synaptic Impairment, Robustness of Excitatory NNs w/ Different Topologies (Mirzakhalili et al 2017)
"Synaptic deficiencies are a known hallmark of neurodegenerative diseases, but the diagnosis of impaired synapses on the cellular level is not an easy task. Nonetheless, changes in the system-level dynamics of neuronal networks with damaged synapses can be detected using techniques that do not require high spatial resolution. This paper investigates how the structure/topology of neuronal networks influences their dynamics when they suffer from synaptic loss. We study different neuronal network structures/topologies by specifying their degree distributions. The modes of the degree distribution can be used to construct networks that consist of rich clubs and resemble small world networks, as well. We define two dynamical metrics to compare the activity of networks with different structures: persistent activity (namely, the self-sustained activity of the network upon removal of the initial stimulus) and quality of activity (namely, percentage of neurons that participate in the persistent activity of the network). Our results show that synaptic loss affects the persistent activity of networks with bimodal degree distributions less than it affects random networks. ..."
412. Synaptic information transfer in computer models of neocortical columns (Neymotin et al. 2010)
"... We sought to measure how the activity of the network alters information flow from inputs to output patterns. Information handling by the network reflected the degree of internal connectivity. ... With greater connectivity strength, the recurrent network translated activity and information due to contribution of activity from intrinsic network dynamics. ... At still higher internal synaptic strength, the network corrupted the external information, producing a state where little external information came through. The association of increased information retrieved from the network with increased gamma power supports the notion of gamma oscillations playing a role in information processing."
413. Synaptic plasticity can produce and enhance direction selectivity (Carver et al, 2008)
" ... We propose a parsimonious model of motion processing that generates direction selective responses using short-term synaptic depression and can reproduce salient features of direction selectivity found in a population of neurons in the midbrain of the weakly electric fish Eigenmannia virescens. The model achieves direction selectivity with an elementary Reichardt motion detector: information from spatially separated receptive fields converges onto a neuron via dynamically different pathways. In the model, these differences arise from convergence of information through distinct synapses that either exhibit or do not exhibit short-term synaptic depression—short-term depression produces phase-advances relative to nondepressing synapses. ..."
414. Synaptic scaling balances learning in a spiking model of neocortex (Rowan & Neymotin 2013)
Learning in the brain requires complementary mechanisms: potentiation and activity-dependent homeostatic scaling. We introduce synaptic scaling to a biologically-realistic spiking model of neocortex which can learn changes in oscillatory rhythms using STDP, and show that scaling is necessary to balance both positive and negative changes in input from potentiation and atrophy. We discuss some of the issues that arise when considering synaptic scaling in such a model, and show that scaling regulates activity whilst allowing learning to remain unaltered.
415. Synchronicity of fast-spiking interneurons balances medium-spiny neurons (Damodaran et al. 2014)
This study investigates the role of feedforward and feedback inhibition in maintaining the balance between D1 and D2 MSNs of the striatum. The synchronized firing of FSIs are found to be critical in this mechanism and specifically the gap junction connections between FSIs.
416. Synchronization by D4 dopamine receptor-mediated phospholipid methylation (Kuznetsova, Deth 2008)
"We describe a new molecular mechanism of dopamine-induced membrane protein modulation that can tune neuronal oscillation frequency to attention related gamma rhythm. This mechanism is based on the unique ability of D4 dopamine receptors (D4R) to carry out phospholipid methylation (PLM) that may affect the kinetics of ion channels. We show that by deceasing the inertia of the delayed rectifier potassium channel, a transition to 40 Hz oscillations can be achieved. ..."
417. Synchrony by synapse location (McTavish et al. 2012)
This model considers synchrony between mitral cells induced via shared granule cell interneurons while taking into account the spatial constraints of the system. In particular, since inhibitory inputs decay passively along the lateral dendrites, this model demonstrates that an optimal arrangement of the inhibitory synapses will be near the cell bodies of the relevant mitral cells.
418. Systematic integration of data into multi-scale models of mouse primary V1 (Billeh et al 2020)
"Highlights • Two network models of the mouse primary visual cortex are developed and released • One uses compartmental-neuron models and the other point-neuron models • The models recapitulate observations from in vivo experimental data • Simulations identify experimentally testable predictions about cortex circuitry"
419. Temporal integration by stochastic recurrent network (Okamoto et al. 2007)
"Temporal integration of externally or internally driven information is required for a variety of cognitive processes. This computation is generally linked with graded rate changes in cortical neurons, which typically appear during a delay period of cognitive task in the prefrontal and other cortical areas. Here, we present a neural network model to produce graded (climbing or descending) neuronal activity. Model neurons are interconnected randomly by AMPA-receptor–mediated fast excitatory synapses and are subject to noisy background excitatory and inhibitory synaptic inputs. In each neuron, a prolonged afterdepolarizing potential follows every spike generation. Then, driven by an external input, the individual neurons display bimodal rate changes between a baseline state and an elevated firing state, with the latter being sustained by regenerated afterdepolarizing potentials. ..."
420. Thalamic network model of deep brain stimulation in essential tremor (Birdno et al. 2012)
"... Thus the decreased effectiveness of temporally irregular DBS trains is due to long pauses in the stimulus trains, not the degree of temporal irregularity alone. We also conducted computer simulations of neuronal responses to the experimental stimulus trains using a biophysical model of the thalamic network. Trains that suppressed tremor in volunteers also suppressed fluctuations in thalamic transmembrane potential at the frequency associated with cerebellar burst-driver inputs. Clinical and computational findings indicate that DBS suppresses tremor by masking burst-driver inputs to the thalamus and that pauses in stimulation prevent such masking. Although stimulation of other anatomic targets may provide tremor suppression, we propose that the most relevant neuronal targets for effective tremor suppression are the afferent cerebellar fibers that terminate in the thalamus."
421. Thalamic quiescence of spike and wave seizures (Lytton et al 1997)
A phase plane analysis of a two cell interaction between a thalamocortical neuron (TC) and a thalamic reticularis neuron (RE).
422. Thalamic Reticular Network (Destexhe et al 1994)
Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994)
423. Thalamic transformation of pallidal input (Hadipour-Niktarash 2006)
"In Parkinson’s disease, neurons of the internal segment of the globus pallidus (GPi) display the low-frequency tremor-related oscillations. These oscillatory activities are transmitted to the thalamic relay nuclei. Computer models of the interacting thalamocortical (TC) and thalamic reticular (RE) neurons were used to explore how the TC-RE network processes the low-frequency oscillations of the GPi neurons. ..."
424. Thalamo-cortical microcircuit (TCM) (AmirAli Farokhniaee and Madeleine M. Lowery 2021)
This is a model of exaggerated beta rhythm observed in the motor cortex, similar to animal and humans with Parkinson’s disease. It is obtained by manually changing the specific cortical, thalamic and thalamocortical synaptic connections, motivated by the previous studies in the field. More importantly and in addition, it serves as a thalamocortical network model of deep brain stimulation, a therapy used for Parkinson’s disease. We computationally stimulated the layer 5 pyramidal neurons of the cortex by direct injected currents to those pyramidal cells and observed well-known patterns in experimental studies, such as attenuation of the exaggerated beta rhythm, formation of excited and inhibited clusters of neurons in the motor cortex and the optimum value for the stimulation, both in amplitude and frequency domains, to obtain the most attenuated beta rhythm.
425. Thalamocortical and Thalamic Reticular Network (Destexhe et al 1996)
NEURON model of oscillations in networks of thalamocortical and thalamic reticular neurons in the ferret. (more applications for a model quantitatively identical to previous DLGN model; updated for NEURON v4 and above)
426. Thalamocortical augmenting response (Bazhenov et al 1998)
In the cortical model, augmenting responses were more powerful in the "input" layer compared with those in the "output" layer. Cortical stimulation of the network model produced augmenting responses in cortical neurons in distant cortical areas through corticothalamocortical loops and low-threshold intrathalamic augmentation. ... The predictions of the model were compared with in vivo recordings from neurons in cortical area 4 and thalamic ventrolateral nucleus of anesthetized cats. The known intrinsic properties of thalamic cells and thalamocortical interconnections can account for the basic properties of cortical augmenting responses. See reference for details. NEURON implementation note: cortical SU cells are getting slightly too little stimulation - reason unknown.
427. Thalamocortical control of propofol phase-amplitude coupling (Soplata et al 2017)
"The anesthetic propofol elicits many different spectral properties on the EEG, including alpha oscillations (8-12 Hz), Slow Wave Oscillations (SWO, 0.1-1.5 Hz), and dose-dependent phase-amplitude coupling (PAC) between alpha and SWO. Propofol is known to increase GABAA inhibition and decrease H-current strength, but how it generates these rhythms and their interactions is still unknown. To investigate both generation of the alpha rhythm and its PAC to SWO, we simulate a Hodgkin-Huxley network model of a hyperpolarized thalamus and corticothalamic inputs. ..."
428. The activity phase of postsynaptic neurons (Bose et al 2004)
We show, in a simplified network consisting of an oscillator inhibiting a follower neuron, how the interaction between synaptic depression and a transient potassium current in the follower neuron determines the activity phase of this neuron. We derive a mathematical expression to determine at what phase of the oscillation the follower neuron becomes active. This expression can be used to understand which parameters determine the phase of activity of the follower as the frequency of the oscillator is changed. See paper for more.
429. The microcircuits of striatum in silico (Hjorth et al 2020)
"Our aim is to reconstruct a full-scale mouse striatal cellular level model to provide a framework to integrate and interpret striatal data. We represent the main striatal neuronal subtypes, the two types of projection neurons (dSPNs and iSPNs) giving rise to the direct and indirect pathways, the fast-spiking interneurons, the low threshold spiking interneurons, and the cholinergic interneurons as detailed compartmental models, with properties close to their biological counterparts. Both intrastriatal and afferent synaptic inputs (cortex, thalamus, dopamine system) are optimized against existing data, including short-term plasticity. This model platform will be used to generate new hypotheses on striatal function or network dynamic phenomena."
430. The neocortical microcircuit collaboration portal (Markram et al. 2015)
"This portal provides an online public resource of the Blue Brain Project's first release of a digital reconstruction of the microcircuitry of juvenile Rat somatosensory cortex, access to experimental data sets used in the reconstruction, and the resulting models."
431. The origin of different spike and wave-like events (Hall et al 2017)
Acute In vitro models have revealed a great deal of information about mechanisms underlying many types of epileptiform activity. However, few examples exist that shed light on spike and wave (SpW) patterns of pathological activity. SpW are seen in many epilepsy syndromes, both generalised and focal, and manifest across the entire age spectrum. They are heterogeneous in terms of their severity, symptom burden and apparent anatomical origin (thalamic, neocortical or both), but any relationship between this heterogeneity and underlying pathology remains elusive. Here we demonstrate that physiological delta frequency rhythms act as an effective substrate to permit modelling of SpW of cortical origin and may help to address this issue. ..."
432. The virtual slice setup (Lytton et al. 2008)
"In an effort to design a simulation environment that is more similar to that of neurophysiology, we introduce a virtual slice setup in the NEURON simulator. The virtual slice setup runs continuously and permits parameter changes, including changes to synaptic weights and time course and to intrinsic cell properties. The virtual slice setup permits shocks to be applied at chosen locations and activity to be sampled intra- or extracellularly from chosen locations. ..."
433. Theory of sequence memory in neocortex (Hawkins & Ahmad 2016)
"... First we show that a neuron with several thousand synapses segregated on active dendrites can recognize hundreds of independent patterns of cellular activity even in the presence of large amounts of noise and pattern variation. We then propose a neuron model where patterns detected on proximal dendrites lead to action potentials, defining the classic receptive field of the neuron, and patterns detected on basal and apical dendrites act as predictions by slightly depolarizing the neuron without generating an action potential. By this mechanism, a neuron can predict its activation in hundreds of independent contexts. We then present a network model based on neurons with these properties that learns time-based sequences. ..."
434. Tonic-clonic transitions in a seizure simulation (Lytton and Omurtag 2007)
"... The authors have ... computationally manageable networks of moderate size consisting of 1,000 to 3,000 neurons with multiple intrinsic and synaptic properties. Experiments on these simulations demonstrated the presence of epileptiform behavior in the form of repetitive high-intensity population events (clonic behavior) or latch-up with near maximal activity (tonic behavior). ... Several simulations revealed the importance of random coincident inputs to shift a network from a low-activation to a high-activation epileptiform state. Finally, a simulated anticonvulsant acting on excitability tended to preferentially decrease tonic activity."
435. Towards a virtual C. elegans (Palyanov et al. 2012)
"... Here we present a detailed demonstration of a virtual C. elegans aimed at integrating these data in the form of a 3D dynamic model operating in a simulated physical environment. Our current demonstration includes a realistic flexible worm body model, muscular system and a partially implemented ventral neural cord. Our virtual C. elegans demonstrates successful forward and backward locomotion when sending sinusoidal patterns of neuronal activity to groups of motor neurons. ..."
436. Translating network models to parallel hardware in NEURON (Hines and Carnevale 2008)
Shows how to move a working network model written in NEURON from a serial processor to a parallel machine in such a way that the final result will produce numerically identical results on either serial or parallel hardware.
437. Turtle visual cortex model (Nenadic et al. 2003, Wang et al. 2005, Wang et al. 2006)
This is a model of the visual cortex of freshwater turtles that is based upon the known anatomy and physiology of individual neurons. The model was published in three papers (Nenadic et al., 2003; Wang et al., 2005; Wang et al., 2006), which should be consulted for full details on its construction. The model has also been used in several papers (Robbins and Senseman, 2004; Du et al., 2005; Du et al., 2006). It is implemented in GENESIS (Bower and Beeman, 1998).
438. Two-cell inhibitory network bursting dynamics captured in a one-dimensional map (Matveev et al 2007)
" ... Here we describe a simple method that allows us to investigate the existence and stability of anti-phase bursting solutions in a network of two spiking neurons, each possessing a T-type calcium current and coupled by reciprocal inhibition. We derive a one-dimensional map which fully characterizes the genesis and regulation of anti-phase bursting arising from the interaction of the T-current properties with the properties of synaptic inhibition. ..."
439. Unbalanced peptidergic inhibition in superficial cortex underlies seizure activity (Hall et al 2015)
" ...Loss of tonic neuromodulatory excitation, mediated by nicotinic acetylcholine or serotonin (5HT3A) receptors, of 5HT3-immunopositive interneurons caused an increase in amplitude and slowing of the delta rhythm until each period became the "wave" component of the spike and wave discharge. As with the normal delta rhythm, the wave of a spike and wave discharge originated in cortical layer 5. In contrast, the "spike" component of the spike and wave discharge originated from a relative failure of fast inhibition in layers 2/3-switching pyramidal cell action potential outputs from single, sparse spiking during delta rhythms to brief, intense burst spiking, phase-locked to the field spike. The mechanisms underlying this loss of superficial layer fast inhibition, and a concomitant increase in slow inhibition, appeared to be precipitated by a loss of neuropeptide Y (NPY)-mediated local circuit inhibition and a subsequent increase in vasoactive intestinal peptide (VIP)-mediated disinhibition. Blockade of NPY Y1 receptors was sufficient to generate spike and wave discharges, whereas blockade of VIP receptors almost completely abolished this form of epileptiform activity. These data suggest that aberrant, activity-dependent neuropeptide corelease can have catastrophic effects on neocortical dynamics."
440. Understanding odor information segregation in the olfactory bulb by MC/TCs (Polese et al. 2014)
Odor identification is one of the main tasks of the olfactory system. It is performed almost independently from the concentration of the odor providing a robust recognition. This capacity to ignore concentration information does not preclude the olfactory system from estimating concentration itself. Significant experimental evidence has indicated that the olfactory system is able to infer simultaneously odor identity and intensity. However, it is still unclear at what level or levels of the olfactory pathway this segregation of information occurs. In this work, we study whether this odor information segregation is performed at the input stage of the olfactory bulb: the glomerular layer.
441. Universal feature of developing networks (Tabak et al 2010)
"Spontaneous episodic activity is a fundamental mode of operation of developing networks. Surprisingly, the duration of an episode of activity correlates with the length of the silent interval that precedes it, but not with the interval that follows. ... We thus developed simple models incorporating excitatory coupling between heterogeneous neurons and activity-dependent synaptic depression. These models robustly generated episodic activity with the correct correlation pattern. The correlation pattern resulted from episodes being triggered at random levels of recovery from depression while they terminated around the same level of depression. To explain this fundamental difference between episode onset and termination, we used a mean field model, where only average activity and average level of recovery from synaptic depression are considered. ... This work further shows that networks with widely different architectures, different cell types, and different functions all operate according to the same general mechanism early in their development."
442. Updated Tritonia Swim CPG (Calin-Jagemann et al. 2007)
Model of the 3-cell core CPG (DSI, C2, and VSI-B) mediating escape swimming in Tritonia diomedea. Cells use a hybrid integrate-and-fire scheme pioneered by Peter Getting. Each model cell is reconstructed from extensive physiological measurements to precisely mimic I-F curves, synaptic waveforms, and functional connectivity.
443. Vertical System (VS) tangential cells network model (Trousdale et al. 2014)
Network model of the VS tangential cell system, with 10 cells per hemisphere. Each cell is a two compartment model with one compartment for dendrites and one for the axon. The cells are coupled through axonal gap junctions. The code allows to simulate responses of the VS network to a variety of visual stimuli to investigate coding as a function of gap junction strength.
444. Vestibulo-Ocular Reflex model in Matlab (Clopath at al. 2014)
" ... We then introduce a minimal model that consists of learning at the parallel fibers to Purkinje cells with the help of the climbing fibers. Although the minimal model reproduces the behavior of the wild-type animals and is analytically tractable, it fails at reproducing the behavior of mutant mice and the electrophysiology data. Therefore, we build a detailed model involving plasticity at the parallel fibers to Purkinje cells' synapse guided by climbing fibers, feedforward inhibition of Purkinje cells, and plasticity at the mossy fiber to vestibular nuclei neuron synapse. The detailed model reproduces both the behavioral and electrophysiological data of both the wild-type and mutant mice and allows for experimentally testable predictions. "
445. Vibration-sensitive Honeybee interneurons (Ai et al 2017)
"Female honeybees use the “waggle dance” to communicate the location of nectar sources to their hive mates. Distance information is encoded in the duration of the waggle phase (von Frisch, 1967). During the waggle phase, the dancer produces trains of vibration pulses, which are detected by the follower bees via Johnston's organ located on the antennae. To uncover the neural mechanisms underlying the encoding of distance information in the waggle dance follower, we investigated morphology, physiology, and immunohistochemistry of interneurons arborizing in the primary auditory center of the honeybee (Apis mellifera). We identified major interneuron types, named DL-Int-1, DL-Int-2, and bilateral DL-dSEG-LP, that responded with different spiking patterns to vibration pulses applied to the antennae. Experimental and computational analyses suggest that inhibitory connection plays a role in encoding and processing the duration of vibration pulse trains in the primary auditory center of the honeybee."
446. Virtual Retina: biological retina simulator, with contrast gain control (Wohrer and Kornprobst 2009)
"We propose a new retina simulation software, called Virtual Retina, which transforms a video into spike trains. Our goal is twofold: Allow large scale simulations (up to 100,000 neurons) in reasonable processing times and keep a strong biological plausibility, taking into account implementation constraints. ... This software will be an evolutionary tool for neuroscientists that need realistic large-scale input spike trains in subsequent treatments, and for educational purposes."
447. Visual physiology of the layer 4 cortical circuit in silico (Arkhipov et al 2018)
"Despite advances in experimental techniques and accumulation of large datasets concerning the composition and properties of the cortex, quantitative modeling of cortical circuits under in-vivo-like conditions remains challenging. Here we report and publicly release a biophysically detailed circuit model of layer 4 in the mouse primary visual cortex, receiving thalamo- cortical visual inputs. The 45,000-neuron model was subjected to a battery of visual stimuli, and results were compared to published work and new in vivo experiments. ..."
448. Working memory circuit with branched dendrites (Morita 2008)
This is a rate-coding model of the neocortical spatial working memory circuit incorporating multiple dendritic branches of the individual pyramidal cell in order to examine how nonlinear dendritic integration, combined with the nonuniform distribution of the external input, affects the behavior of the whole circuit.

Re-display model names without descriptions