Circuits that contain the Region : Hippocampus

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    Models   Description
1. A computational model of systems memory consolidation and reconsolidation (Helfer & Shultz 2019)
A neural-network framework for modeling systems memory consolidation and reconsolidation.
2. A NN with synaptic depression for testing the effects of connectivity on dynamics (Jacob et al 2019)
Here we used a 10,000 neuron model. The neurons are a mixture of excitatory and inhibitory integrate-and-fire neurons connected with synapses that exhibit synaptic depression. Three different connectivity paradigms were tested to look for spontaneous transition between interictal spiking and seizure: uniform, small-world network, and scale-free. All three model types are included here.
3. 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.
4. 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.
5. 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.
6. 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.
7. 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.
8. CRH modulates excitatory transmission and network physiology in hippocampus (Gunn et al. 2017)
This model simulates the effects of CRH on sharp waves in a rat CA1/CA3 model. It uses the frequency of the sharp waves as an output of the network.
9. 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.
10. 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
11. 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.
12. 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.
13. 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.
14. 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). ..."
15. 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.
16. 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.
17. 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. ..."
18. Hierarchical anti-Hebbian network model for the formation of spatial cells in 3D (Soman et al 2019)
This model shows how spatial representations in 3D space could emerge using unsupervised neural networks. Model is a hierarchical one which means that it has multiple layers, where each layer has got a specific function to achieve. This architecture is more of a generalised one i.e. it gives rise to different kinds of spatial representations after training.
19. 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."
20. 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
21. 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).
22. 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.
23. 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.
24. 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."
25. 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. ..."
26. 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"
27. Interplay between somatic and dendritic inhibition promotes place fields (Pedrosa & Clopath 2020)
Hippocampal pyramidal neurons are thought to encode spatial information. A subset of these cells, named place cells, are active only when the animal traverses a specific region within the environment. Although vastly studied experimentally, the development and stabilization of place fields are not fully understood. Here, we propose a mechanistic model of place cell formation in the hippocampal CA1 region. Using our model, we reproduce place field dynamics observed experimentally and provide a mechanistic explanation for the stabilization of place fields. Finally, our model provides specific predictions on protocols to shift place field location.
28. 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. ..."
29. 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."
30. 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.
31. 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. ..."
32. 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. ..."
33. 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.
34. 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."
35. 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. ..."
36. 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."
37. Odor supported place cell model and goal navigation in rodents (Kulvicius et al. 2008)
" ... Here we model odor supported place cells by using a simple feed-forward network and analyze the impact of olfactory cues on place cell formation and spatial navigation. The obtained place cells are used to solve a goal navigation task by a novel mechanism based on self-marking by odor patches combined with a Q-learning algorithm. We also analyze the impact of place cell remapping on goal directed behavior when switching between two environments. ..."
38. 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.
39. 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). ..."
40. Place and grid cells in a loop (Rennó-Costa & Tort 2017)
This model implements a loop circuit between place and grid cells. The model was used to explain place cell remapping and grid cell realignment. Grid cell model as a continuous attractor network. Place cells have recurrent attractor network. Rate models implemented with E%-MAX winner-take-all network dynamics, with gamma cycle time-step.
41. 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.
42. 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.
43. SHOT-CA3, RO-CA1 Training, & Simulation CODE in models of hippocampal replay (Nicola & Clopath 2019)
In this code, we model the interaction between the medial septum and hippocampus as a FORCE trained, dual oscillator model. One oscillator corresponds to the medial septum and serves as an input, while a FORCE trained network of LIF neurons acts as a model of the CA3. We refer to this entire model as the Septal Hippocampal Oscillator Theta (or SHOT) network. The code contained in this upload allows a user to train a SHOT network, train a population of reversion interneurons, and simulate the SHOT-CA3 and RO-CA1 networks after training. The code scripts are labeled to correspond to the figure from the manuscript.
44. 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.
45. 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.

Re-display model names without descriptions