Models that contain the Model Concept : Depression

(Reduction in the amplitude of Excitatory PostSynaptic Potentials following a stimulus train. The amplitude reduction and it's recovery depend on the stimulus and have time constants of a few seconds to a few minutes. Thought to be a presynaptic effect involving the number of quanta.)
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    Models   Description
1.  A Computational Model of Bidirectional Plasticity Regulation by betaCaMKII (Pinto et al. 2019)
We present a computational model that suggests how calcium-calmodulin dependent protein kinase II can act as a molecular switch in synaptic plasticity induction at an important cerebellar synapse (between parallel fibres and Purkinje cells). Our simulation results provide a potential explanation for experimental data by van Woerden et al (Van Woerden G, Hoebeek F, Gao Z, Nagaraja R, Hoogenraad C, Kushner S, et al. [beta]CaMKII controls the direction of plasticity at parallel fiber-Purkinje cell synapses. Nat Neurosci. 2009;12(7):823-825). These experiments were performed in the lab led by Professor Chris De Zeeuw.
2.  A kinetic model unifying presynaptic short-term facilitation and depression (Lee et al. 2009)
"... Here, we propose a unified theory of synaptic short-term plasticity based on realistic yet tractable and testable model descriptions of the underlying intracellular biochemical processes. Analysis of the model equations leads to a closed-form solution of the resonance frequency, a function of several critical biophysical parameters, as the single key indicator of the propensity for synaptic facilitation or depression under repetitive stimuli. This integrative model is supported by a broad range of transient and frequency response experimental data including those from facilitating, depressing or mixed-mode synapses. ... the model provides the reasons behind the switching behavior between facilitation and depression observed in experiments. ..."
3.  Adaptation of Short-Term Plasticity parameters (Esposito et al. 2015)
"The anatomical connectivity among neurons has been experimentally found to be largely non-random across brain areas. This means that certain connectivity motifs occur at a higher frequency than would be expected by chance. Of particular interest, short-term synaptic plasticity properties were found to colocalize with specific motifs: an over-expression of bidirectional motifs has been found in neuronal pairs where short-term facilitation dominates synaptic transmission among the neurons, whereas an over-expression of unidirectional motifs has been observed in neuronal pairs where short-term depression dominates. In previous work we found that, given a network with fixed short-term properties, the interaction between short- and long-term plasticity of synaptic transmission is sufficient for the emergence of specific motifs. Here, we introduce an error-driven learning mechanism for short-term plasticity that may explain how such observed correspondences develop from randomly initialized dynamic synapses. ..."
4.  AMPA receptor trafficking and its role in heterosynaptic plasticity (Antunes et al 2018)
"... cumulative experimental and theoretical data have demonstrated that long-term potentiation (LTP) and long-term depression (LTD) can promote compensatory alterations in non-stimulated synapses. In this work, we have developed a (MCELL) computational model of a (3D) spiny dendritic segment to investigate the role of AMPA receptor (AMPAR) trafficking during synaptic plasticity at specific synapses and its consequences for the populations of AMPAR at nearby synapses. Our results demonstrated that the mechanisms of AMPAR trafficking involved with LTP and LTD can promote heterosynaptic plasticity at non-stimulated synapses. These alterations are compensatory and arise from molecular competition. Moreover, the heterosynaptic changes observed in our model can modulate further activity-driven inductions of synaptic plasticity." The model requires an installed version of MCell and CellBlender.
5.  Amyloid-beta effects on release probability and integration at CA3-CA1 synapses (Romani et al. 2013)
The role of amyloid beta (Aß) in brain function and in the pathogenesis of Alzheimer’s disease remains elusive. Recent publications reported that an increase in Aß concentration perturbs presynaptic release in hippocampal neurons, in particular by increasing release probability of CA3-CA1 synapses. The model predics how this alteration can affect synaptic plasticity and signal integration. The results suggest that the perturbation of release probability induced by increased Aß can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during Alzheimer’s disease.
6.  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.
7.  CA1 pyramidal neuron: as a 2-layer NN and subthreshold synaptic summation (Poirazi et al 2003)
We developed a CA1 pyramidal cell model calibrated with a broad spectrum of in vitro data. Using simultaneous dendritic and somatic recordings, and combining results for two different response measures (peak vs. mean EPSP), two different stimulus formats (single shock vs. 50 Hz trains), and two different spatial integration conditions (within vs. between-branch summation), we found the cell's subthreshold responses to paired inputs are best described as a sum of nonlinear subunit responses, where the subunits correspond to different dendritic branches. In addition to suggesting a new type of experiment and providing testable predictions, our model shows how conclusions regarding synaptic arithmetic can be influenced by an array of seemingly innocuous experimental design choices.
8.  High entrainment constrains synaptic depression in a globular bushy cell (Rudnicki & Hemmert 2017)
" ... Here we show how different levels of synaptic depression shape firing properties of GBCs in in vivo-like conditions using computer simulations. We analyzed how an interplay of synaptic depression (0 % to 70 %) and the number of auditory nerve fiber inputs (10 to 70) contributes to the variability of the experimental data from previous studies. ... Overall, this study helps to understand how synaptic properties shape temporal processing in the auditory system. It also integrates, compares, and reconciles results of various experimental studies."
9.  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.
10.  Human layer 2/3 cortical microcircuits in health and depression (Yao et al, 2022)
11.  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. ..."
12.  Model of cerebellar parallel fiber-Purkinje cell LTD and LTP (Gallimore et al 2018)
Model of cerebellar parallel fiber-Purkinje cell LTD and LTP implemented in Matlab Simbiology
13.  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."
14.  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.
15.  Short term plasticity of synapses onto V1 layer 2/3 pyramidal neuron (Varela et al 1997)
This archive contains 3 mod files for NEURON that implement the short term synaptic plasticity model described in Varela, J.A., Sen, K., Gibson, J., Fost, J., Abbott, L.R., and Nelson, S.B.. A quantitative description of short-term plasticity at excitatory synapses in layer 2/3 of rat primary visual cortex. Journal of Neuroscience 17:7926-7940, 1997. Contact if you have questions about this implementation of the model.
16.  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.
17.  Spike timing detection in different forms of LTD (Doi et al 2005)
To understand the spike-timing detection mechanisms in cerebellar long-term depression (LTD), we developed a kinetic model of Ca dynamics within a Purkinje dendritic spine. In our kinetic simulation, IP3 was first produced via the metabotropic pathway of parallel fiber (PF) inputs, and the Ca influx in response to the climbing fiber (CF) input triggered regenerative Ca-induced Ca release from the internal stores via the IP3 receptors activated by the increased IP3. The delay in IP3 increase caused by the PF metabotropic pathway generated the optimal PF–CF interval. The Ca dynamics revealed a threshold for large Ca2 release that decreased as IP3 increased, and it coherently explained the different forms of LTD. See paper for more and details.
18.  Stochastic LTP/LTD conditioning of a synapse (Migliore and Lansky 1999)
Protracted presynaptic activity can induce long-term potentiation (LTP) or long-term depression (LTD) of the synaptic strength. However, virtually all the experiments testing how LTP and LTD depend on the conditioning input are carried out with trains of stimuli at constant frequencies, whereas neurons in vivo most likely experience a stochastic variation of interstimulus intervals. We used a computational model of synaptic transmission to test if and to what extent the stochastic fluctuations of an input signal could alter the probability to change the state of a synapse. See paper for conclusions.
19.  Synaptic damage underlies EEG abnormalities in postanoxic encephalopathy (Ruijter et al 2017)
"... In postanoxic coma, EEG patterns indicate the severity of encephalopathy and typically evolve in time. We aim to improve the understanding of pathophysiological mechanisms underlying these EEG abnormalities. ... We used a mean field model comprising excitatory and inhibitory neurons, local synaptic connections, and input from thalamic afferents. Anoxic damage is modeled as aggravated short-term synaptic depression, with gradual recovery over many hours. Additionally, excitatory neurotransmission is potentiated, scaling with the severity of anoxic encephalopathy. Simulations were compared with continuous EEG recordings of 155 comatose patients after cardiac arrest. ..."
20.  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. ..."
21.  Synaptic plasticity: pyramid->pyr and pyr->interneuron (Tsodyks et al 1998)
An implementation of a model of short-term synaptic plasticity with NEURON. The model was originally described by Tsodyks et al., who assumed that the synapse acted as a current source, but this implementation treats it as a conductance change. Tsodyks, M., Pawelzik, K., Markram, H. Neural networks with dynamic synapses. Neural Computation 10:821-835, 1998. Tsodyks, M., Uziel, A., Markram, H. Synchrony generation in recurrent networks with frequency-dependent synapses. J. Neurosci. 2000 RC50.
22.  Synaptic transmission at the calyx of Held (Graham et al 2001)
This model allows the user to investigate faciliation and depression in a complex Monte Carlo model of the calyx of Held, a giant synapse in the mammalian auditory system (Graham et al, 2001)

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