Models that contain the Model Concept : Homeostasis

(Cellular mechanisms where the activity of a cell is maintained, e.g. the electrical activity of a cell is maintained by the insertion and removal or activation and inactivation (through phosphorylation or other means) of intrinsic currents and synaptic receptors.)
Re-display model names without descriptions
    Models   Description
1.  Activity dependent conductances in a neuron model (Liu et al. 1998)
"... We present a model of a stomatogastric ganglion (STG) neuron in which several Ca2+-dependent pathways are used to regulate the maximal conductances of membrane currents in an activity-dependent manner. Unlike previous models of this type, the regulation and modification of maximal conductances by electrical activity is unconstrained. The model has seven voltage-dependent membrane currents and uses three Ca2+ sensors acting on different time scales. ... The model suggests that neurons may regulate their conductances to maintain fixed patterns of electrical activity, rather than fixed maximal conductances, and that the regulation process requires feedback systems capable of reacting to changes of electrical activity on a number of different time scales."
2.  Anoxic depolarization, recovery: effect of brain regions and extracellular space (Hubel et al. 2016)
The extent of anoxic depolarization (AD), the initial electrophysiological event during ischemia, determines the degree of brain region-specific neuronal damage. Neurons in higher brain regions have stronger ADs and are more easily injured than neurons in lower brain region. The mechanism leading to such differences is not clear. We use a computational model based on a Hodgkin-Huxley framework which includes neural spiking dynamics, processes of ion accumulation, and homeostatic mechanisms like vascular coupling and Na/K-exchange pumps. We show that a large extracellular space (ECS) explains the recovery failure in high brain regions. A phase-space analysis shows that with a large ECS recovery from AD through potassium regulation is impossible. The code 'time_series.ode' can be used to simulate AD for a large and a small ECS and show the different behaviors. The code ‘continuations.ode’ can be used to show the fixed point structure. Depending on our choice of large or small ECS the fixed point curve implies the presence/absence of a recovery threshold that defines the potassium clearance demand.
3.  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. ..."
4.  DCN fusiform cell (Ceballos et al. 2016)
Dorsal cochlear nucleus principal neurons, fusiform neurons, display heterogeneous spontaneous action potential activity and thus represent an appropriate model to study the role of different conductances in establishing firing heterogeneity. Particularly, fusiform neurons are divided into quiet, with no spontaneous firing, or active neurons, presenting spontaneous, regular firing. These modes are determined by the expression levels of an intrinsic membrane conductance, an inwardly rectifying potassium current (IKir). We used a computational model to test whether other subthreshold conductances vary homeostatically to maintain membrane excitability constant across the two subtypes. We found that Ih expression covaries specifically with IKir in order to maintain membrane resistance constant. The impact of Ih on membrane resistance is dependent on the level of IKir expression, being much smaller in quiet neurons with bigger IKir, but Ih variations are not relevant for creating the quiet and active phenotypes. We conclude that in fusiform neurons the variations of their different subthreshold conductances are limited to specific conductances in order to create firing heterogeneity and maintain membrane homeostasis.
5.  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. ...
6.  Differential interactions between Notch and ID factors control neurogenesis (Boareto et al 2017)
"During embryonic and adult neurogenesis, neural stem cells (NSCs) generate the correct number and types of neurons in a temporospatial fashion. Control of NSC activity and fate is crucial for brain formation and homeostasis. Neurogenesis in the embryonic and adult brain differ considerably, but Notch signaling and inhibitor of DNA-binding (ID) factors are pivotal in both. Notch and ID factors regulate NSC maintenance; however, it has been difficult to evaluate how these pathways potentially interact. Here, we combined mathematical modeling with analysis of single-cell transcriptomic data to elucidate unforeseen interactions between the Notch and ID factor pathways. ..."
7.  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.
8.  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. ... "
9.  Feedforward network undergoing Up-state-mediated plasticity (Gonzalez-Rueda et al. 2018)
Using whole-cell recordings and optogenetic stimulation of presynaptic input in anaesthetized mice, we show that synaptic plasticity rules are gated by cortical dynamics. Up states are biased towards depression such that presynaptic stimulation alone leads to synaptic depression, while connections contributing to postsynaptic spiking are protected against this synaptic weakening. We find that this novel activity-dependent and input-specific downscaling mechanism has two important computational advantages: 1) improved signal-to-noise ratio, and 2) preservation of previously stored information. Thus, these synaptic plasticity rules provide an attractive mechanism for SWS-related synaptic downscaling and circuit refinement. We simulate a feedforward network of neurons undergoing Up-state-mediated plasticity. Under this plasticity rule, presynaptic spikes alone lead to synaptic depression, whereas those followed by postsynaptic spikes within 10 ms are not changed.
10.  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.
11.  Genetic, biochemical and bioelectrical dynamics in pattern regulation (Pietak & Levin 2017)
"Gene regulatory networks (GRNs) describe interactions between gene products and transcription factors that control gene expression. In combination with reaction–diffusion models, GRNs have enhanced comprehension of biological pattern formation. However, although it is well known that biological systems exploit an interplay of genetic and physical mechanisms, instructive factors such as transmembrane potential (Vmem) have not been integrated into full GRN models. Here we extend regulatory networks to include bioelectric signalling, developing a novel synthesis: the bioelectricity-integrated gene and reaction (BIGR) network. ..."
12.  Hodgkin-Huxley with dynamic ion concentrations (Hubel and Dahlem, 2014)
The classical Hodgkin--Huxley (HH) model neglects the time-dependence of ion concentrations in spiking dynamics. The dynamics is therefore limited to a time scale of milliseconds, which is determined by the membrane capacitance multiplied by the resistance of the ion channels, and by the gating time constants. This model includes slow dynamics in an extended HH framework that simulates time-dependent ion concentrations, pumps, and buffers. Fluxes across the neuronal membrane change intra- and extracellular ion concentrations, whereby the latter can also change through contact to reservoirs in the surroundings. The dynamics on three distinct slow times scales is determined by the cell volume-to-surface-area ratio and the membrane permeability (seconds), the buffer time constants (tens of seconds), and the slower backward buffering (minutes to hours). The modulatory dynamics and the newly emerging excitable dynamics corresponds to pathological conditions observed in epileptiform burst activity, and spreading depression in migraine aura and stroke, respectively.
13.  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).
14.  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.
15.  Modeling dentate granule cells heterosynaptic plasticity using STDP-BCM rule (Jedlicka et al. 2015)
... Here we study how key components of learning mechanisms in the brain, namely spike timing-dependent plasticity and metaplasticity, interact with spontaneous activity in the input pathways of the neuron. Using biologically realistic simulations we show that ongoing background activity is a key determinant of the degree of long-term potentiation and long-term depression of synaptic transmission between nerve cells in the hippocampus of freely moving animals. This work helps better understand the computational rules which drive synaptic plasticity in vivo. ...
16.  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. ..."
17.  Multiscale interactions between chemical and electric signaling in LTP (Bhalla 2011)
"Synaptic plasticity leads to long-term changes in excitability, whereas cellular homeostasis maintains excitability. Both these processes involve interactions between molecular events, electrical events, and network activity. Here I explore these intersections with a multilevel model that embeds molecular events following synaptic calcium influx into a multicompartmental electrical model of a CA1 hippocampal neuron. ..."
18.  Nodes of Ranvier with left-shifted Nav channels (Boucher et al. 2012)
The two programs CLSRanvier.f and propagation.f simulate the excitability of a myelinated axon with injured nodes of Ranvier. The injury is simulated as the Coupled Left Shift (CLS) of the activation(V) and inactivation(V) (availability) of a fraction of Nav channels.
19.  Optimal balance predicts/explains amplitude and decay time of iPSGs (Kim & Fiorillo 2017)
"Synaptic inhibition counterbalances excitation, but it is not known what constitutes optimal inhibition. We previously proposed that perfect balance is achieved when the peak of an excitatory postsynaptic potential (EPSP) is exactly at spike threshold, so that the slightest variation in excitation determines whether a spike is generated. Using simulations, we show that the optimal inhibitory postsynaptic conductance (IPSG) increases in amplitude and decay rate as synaptic excitation increases from 1 to 800 Hz. As further proposed by theory, we show that optimal IPSG parameters can be learned through anti-Hebbian rules. ..."
20.  Quantitative model of sleep-wake dynamics (Phillips & Robinson 2007)
"A quantitative, physiology-based model of the ascending arousal system is developed, using continuum neuronal population modeling, which involves averaging properties such as firing rates across neurons in each population. The model includes the ventrolateral preoptic area (VLPO), where circadian and homeostatic drives enter the system, the monoaminergic and cholinergic nuclei of the ascending arousal system, and their interconnections. The human sleep-wake cycle is governed by the activities of these nuclei, which modulate the behavioral state of the brain via diffuse neuromodulatory projections. ... The model behavior is robust across the constrained parameter ranges, but with sufficient flexibility to describe a wide range of observed phenomena. "
21.  Sleep deprivation in the ascending arousal system (Phillips & Robinson 2008)
"A physiologically based quantitative model of the human ascending arousal system is used to study sleep deprivation after being calibrated on a small set of experimentally based criteria. The model includes the sleep–wake switch of mutual inhibition between nuclei which use monoaminergic neuromodulators, and the ventrolateral preoptic area. The system is driven by the circadian rhythm and sleep homeostasis. We use a small number of experimentally derived criteria to calibrate the model for sleep deprivation, then investigate model predictions for other experiments, demonstrating the scope of application. ... The form of the homeostatic drive suggests that periods of wake during recovery from sleep deprivation are phases of relative recovery, in the sense that the homeostatic drive continues to converge toward baseline levels. This undermines the concept of sleep debt, and is in agreement with experimentally restricted recovery protocols. Finally, we compare our model to the two-process model, and demonstrate the power of physiologically based modeling by correctly predicting sleep latency times following deprivation from experimental data. "
22.  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.
23.  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.
24.  The role of glutamate in neuronal ion homeostasis: spreading depolarization (Hubel et al 2017)
This model includes ion concentration dynamics (sodium, potassium, chloride) inside and outside the neuron, the exchange of ions with glia and blood vessels, volume dynamics of neuron, glia, and extracellular space, glutamate homeostasis involving release by neuron and uptake by both neuron and glia. Spreading depolarization is used as a case study.
25.  TRPM8-dependent dynamic response in cold thermoreceptors (Olivares et al. 2015)
This model reproduces the dynamic response of cold thermoreceptors, transiently changing the firing rate upon heating or cooling. It also displays the 'static' or adapted firing patterns observed in these receptors.

Re-display model names without descriptions