Circuits that contain the Neuron : Neocortex L5/6 pyramidal GLU cell

(The cell bodies (somas) of these projection neurons are found in the (deeper) layers 5/6 of cortex, and have a pyramid shape. These cells release glutamate, the most common excitatory neurotransmitter. These are corticothalamic (project to the thalamus), pyramidal tract (project to the brain stem and spinal cord), and intratelencephalic (project to the cortex, possibly the other hemisphere, or the basal ganglia). Where the axon goes determines these additional classes. The apical tuft is thicker for the subtypes of these cells primarily in layer 5b (deeper layer 5) that project to subcortical regions and thinner for those in layer 5a (superficial layer 5) that project through the corpus callosum to the other hemisphere.)
Re-display model names without descriptions
    Models   Description
1. A neural mass model for critical assessment of brain connectivity (Ursino et al 2020)
We use a neural mass model of interconnected regions of interest to simulate reliable neuroelectrical signals in the cortex. In particular, signals simulating mean field potentials were generated assuming two, three or four ROIs, connected via excitatory or by-synaptic inhibitory links. Then we investigated whether bivariate Transfer Entropy (TE) can be used to detect a statistically significant connection from data (as in binary 0/1 networks), and even if connection strength can be quantified (i.e., the occurrence of a linear relationship between TE and connection strength). Results suggest that TE can reliably estimate the strength of connectivity if neural populations work in their linear regions. However, nonlinear phenomena dramatically affect the assessment of connectivity, since they may significantly reduce TE estimation. Software included here allows the simulation of neural mass models with a variable number of ROIs and connections, the estimation of TE using the free package Trentool, and the realization of figures to compare true connectivity with estimated values.
2. 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. "
3. 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. ..."
4. 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. ..."
5. 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."
6. 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."
7. 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. ... "
8. 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).
9. 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. ..."
10. 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."
11. 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.
12. 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.
13. 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="">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 .
14. L5 PFC microcircuit used to study persistent activity (Papoutsi et al. 2014, 2013)
Using a heavily constrained biophysical model of a L5 PFC microcircuit we investigate the mechanisms that underlie persistent activity emergence (ON) and termination (OFF) and search for the minimum network size required for expressing these states within physiological regimes.
15. 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. ..."
16. 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.
17. 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.
18. 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. ..."
19. 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
20. 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."
21. 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. "
22. 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."
23. Multiscale model of primary motor cortex circuits predicts in vivo dynamics (Dura-Bernal et al 2023)
Understanding cortical function requires studying multiple scales: molecular, cellular, circuit and behavior. We developed a multiscale biophysically-detailed model of mouse primary motor cortex (M1) with over 10,000 neurons and 30 million synapses. Neuron types, densities, spatial distributions, morphologies, biophysics, connectivity and dendritic synapse locations were constrained by experimental data. The model includes long-range inputs from seven thalamic and cortical regions, and noradrenergic inputs. Connectivity depends on cell class and cortical depth at sublaminar resolution. The model accurately predicted in vivo layer- and cell type-specific responses (firing rates and LFP) associated with behavioral states (quiet wakefulness and movement) and experimental manipulations (noradrenaline receptor blockade and thalamus inactivation). We generated mechanistic hypotheses underlying the observed activity and analyzed low-dimensional population latent dynamics. This quantitative theoretical framework can be used to integrate and interpret M1 experimental data and sheds light on the cell type-specific multiscale dynamics associated with several experimental conditions and behaviors.
24. 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. ..."
25. 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.
26. 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.
27. Neural Mass Model for relationship between Brain Rhythms + Functional Connectivity (Ricci et al '21)
The Neural Mass Model (NMM) generates biologically reliable mean field potentials of four interconnected regions of interest (ROIs) of the cortex, each simulating a different brain rhythm (in theta, alpha, beta and gamma ranges). These neuroelectrical signals originate from the assumption that ROIs influence each other via of excitatory or by-synaptic inhibitory connections. Besides receiving long-range synapses from other ROIs, each one receives an external input and superimposed Gaussian white noise. We used the NMM to simulate different connectivity networks of four ROIs, by varying both the synaptic strengths and the inputs. The purpose of this study is to investigate how the transmission of brain rhythms behaves under linear and nonlinear conditions. To this aim, we investigated the performance of eight Functional Connectivity (FC) estimators (Correlation, Delayed Correlation, Coherence, Lagged Coherence, Temporal Granger Causality, Spectral Granger Causality, Phase Synchronization and Transfer Entropy) in detecting the connectivity network changes. Results suggest that when a ROI works in the linear region, its capacity to transmit its rhythm increases, while when it saturates, the oscillatory activity becomes strongly affected by other ROIs. Software included here allows the simulation of mean field potentials of four interconnected ROIs, their visualization, both in time and frequency domains, and the estimation of the related FC with eight different methods (for Transfer Entropy the Trentool package is needed).
28. 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.
29. 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.
30. Prosthetic electrostimulation for information flow repair in a neocortical simulation (Kerr 2012)
This model is an extension of a model ( ) 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.
31. 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.
32. 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. ... "
33. 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.
34. 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. ..."
35. 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.
36. 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. ..."
37. 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.
38. 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.
39. 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."
40. 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.
41. 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. ..."
42. 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"
43. 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.
44. 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. ..."

Re-display model names without descriptions