Models that contain the Model Concept : Calcium dynamics

(Models that include accumulation (and dissipation) of calcium.)
Re-display model names without descriptions
    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 dual-Ca2+-sensor model for neurotransmitter release in a central synapse (Sun et al. 2007)
"Ca2+-triggered synchronous neurotransmitter release is well described, but asynchronous release-in fact, its very existence-remains enigmatic. Here we report a quantitative description of asynchronous neurotransmitter release in calyx-of-Held synapses. ... Our results reveal that release triggered in wild-type synapses at low Ca2+ concentrations is physiologically asynchronous, and that asynchronous release completely empties the readily releasable pool of vesicles during sustained elevations of Ca2+. We propose a dual-Ca2+-sensor model of release that quantitatively describes the contributions of synchronous and asynchronous release under conditions of different presynaptic Ca2+ dynamics."
3.  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. ..."
4.  A mathematical model of a neurovascular unit (Dormanns et al 2015, 2016) (Farrs & David 2011)
Here a lumped parameter numerical model of a neurovascular unit is presented, representing an intercellular communication system based on ion exchange through pumps and channels between neurons, astrocytes, smooth muscle cells, endothelial cells, and the spaces between these cells: the synaptic cleft between the neuron and astrocyte, the perivascular space between the astrocyte and SMC, and the extracellular space surrounding the cells. The model contains various cellular and chemical pathways such as potassium, astrocytic calcium, and nitric oxide. The model is able to simulate neurovascular coupling, the process characterised by an increase in neuronal activity followed by a rapid dilation of local blood vessels and hence increased blood supply providing oxygen and glucose to cells in need.
5.  A mathematical model of evoked calcium dynamics in astrocytes (Handy et al 2017)
" ...Here we present a qualitative analysis of a recent mathematical model of astrocyte calcium responses. We show how the major response types are generated in the model as a result of the underlying bifurcation structure. By varying key channel parameters, mimicking blockers used by experimentalists, we manipulate this underlying bifurcation structure and predict how the distributions of responses can change. We find that store-operated calcium channels, plasma membrane bound channels with little activity during calcium transients, have a surprisingly strong effect, underscoring the importance of considering these channels in both experiments and mathematical settings. ..."
6.  A model of neurovascular coupling and the BOLD response (Mathias et al 2017, Kenny et al 2018)
Here a lumped parameter numerical model of a neurovascular unit is presented, representing an intercellular communication system based on ion exchange through pumps and channels between neurons, astrocytes, smooth muscle cells, endothelial cells, and the spaces between these cells: the synaptic cleft between the neuron and astrocyte, the perivascular space between the astrocyte and SMC, and the extracellular space surrounding the cells. The model contains various cellular and chemical pathways such as potassium, astrocytic calcium, and nitric oxide. The model is able to simulate neurovascular coupling, the process characterised by an increase in neuronal activity followed by a rapid dilation of local blood vessels and hence increased blood supply providing oxygen and glucose to cells in need. The model also incorporates the BOLD response.
7.  A multiscale approach to analyze circadian rhythms (Vasalou & Henson, 2010) (CellML)
" ... We developed a firing rate code model to incorporate known electrophysiological properties of SCN (suprachiasmatic nucleus) pacemaker cells, including circadian dependent changes in membrane voltage and ion conductances. Calcium dynamics were included in the model as the putative link between electrical firing and gene expression. Individual ion currents exhibited oscillatory patterns matching experimental data both in current levels and phase relationships. VIP and GABA neurotransmitters, which encode synaptic signals across the SCN, were found to play critical roles in daily oscillations of membrane excitability and gene expression. Blocking various mechanisms of intracellular calcium accumulation by simulated pharmacological agents (nimodipine, IP3- and ryanodine-blockers) reproduced experimentally observed trends in firing rate dynamics and core-clock gene transcription. The intracellular calcium concentration was shown to regulate diverse circadian processes such as firing frequency, gene expression and system periodicity. The model predicted a direct relationship between firing frequency and gene expression amplitudes, demonstrated the importance of intracellular pathways for single cell behavior and provided a novel multiscale framework which captured characteristics of the SCN at both the electrophysiological and gene regulatory levels."
8.  A multiscale approach to analyze circadian rhythms (Vasalou & Henson, 2010) (SBML)
" ... We developed a firing rate code model to incorporate known electrophysiological properties of SCN (suprachiasmatic nucleus) pacemaker cells, including circadian dependent changes in membrane voltage and ion conductances. Calcium dynamics were included in the model as the putative link between electrical firing and gene expression. Individual ion currents exhibited oscillatory patterns matching experimental data both in current levels and phase relationships. VIP and GABA neurotransmitters, which encode synaptic signals across the SCN, were found to play critical roles in daily oscillations of membrane excitability and gene expression. Blocking various mechanisms of intracellular calcium accumulation by simulated pharmacological agents (nimodipine, IP3- and ryanodine-blockers) reproduced experimentally observed trends in firing rate dynamics and core-clock gene transcription. The intracellular calcium concentration was shown to regulate diverse circadian processes such as firing frequency, gene expression and system periodicity. The model predicted a direct relationship between firing frequency and gene expression amplitudes, demonstrated the importance of intracellular pathways for single cell behavior and provided a novel multiscale framework which captured characteristics of the SCN at both the electrophysiological and gene regulatory levels."
9.  A set of reduced models of layer 5 pyramidal neurons (Bahl et al. 2012)
These are the NEURON files for 10 different models of a reduced L5 pyramidal neuron. The parameters were obtained by automatically fitting the models to experimental data using a multi objective evolutionary search strategy. Details on the algorithm can be found at http://www.g-node.org/emoo and in Bahl et al. (2012).
10.  A simple integrative electrophysiological model of bursting GnRH neurons (Csercsik et al. 2011)
In this paper a modular model of the GnRH neuron is presented. For the aim of simplicity, the currents corresponding to fast time scales and action potential generation are described by an impulsive system, while the slower currents and calcium dynamics are described by usual ordinary differential equations (ODEs). The model is able to reproduce the depolarizing afterpotentials, afterhyperpolarization, periodic bursting behavior and the corresponding calcium transients observed in the case of GnRH neurons.
11.  Action potential of mouse urinary bladder smooth muscle (Mahapatra et al 2018)
Urinary incontinence is associated with enhanced spontaneous phasic contractions of the detrusor smooth muscle (DSM). Although a complete understanding of the etiology of these spontaneous contractions is not yet established, it is suggested that the spontaneously evoked action potentials (sAPs) in DSM cells initiate and modulate the contractions. In order to further our understanding of the ionic mechanisms underlying sAP generation, we present here a biophysically detailed computational model of a single DSM cell. First, we constructed mathematical models for nine ion channels found in DSM cells based on published experimental data: two voltage-gated Ca2+ ion channels, an hyperpolarization-activated ion channel, two voltage-gated K+ ion channels, three Ca2+-activated K+ ion channels and a non-specific background leak ion channel. Incorporating these channels, our DSM model is capable of reproducing experimentally recorded spike-type sAPs of varying configurations, ranging from sAPs displaying after-hyperpolarizations to sAPs displaying after-depolarizations. Our model, constrained heavily by physiological data, provides a powerful tool to investigate the ionic mechanisms underlying the genesis of DSM electrical activity, which can further shed light on certain aspects of urinary bladder function and dysfunction.
12.  Active dendrites shape signaling microdomains in hippocampal neurons (Basak & Narayanan 2018)
The spatiotemporal spread of biochemical signals in neurons and other cells regulate signaling specificity, tuning of signal propagation, along with specificity and clustering of adaptive plasticity. Theoretical and experimental studies have demonstrated a critical role for cellular morphology and the topology of signaling networks in regulating this spread. In this study, we add a significantly complex dimension to this narrative by demonstrating that voltage-gated ion channels (A-type Potassium channels and T-type Calcium channels) on the plasma membrane could actively amplify or suppress the strength and spread of downstream signaling components. We employed a multiscale, multicompartmental, morphologically realistic, conductance-based model that accounted for the biophysics of electrical signaling and the biochemistry of calcium handling and downstream enzymatic signaling in a hippocampal pyramidal neuron. We chose the calcium – calmodulin – calcium/calmodulin-dependent protein kinase II (CaMKII) – protein phosphatase 1 (PP1) signaling pathway owing to its critical importance to several forms of neuronal plasticity, and employed physiologically relevant theta-burst stimulation (TBS) or theta-burst pairing (TBP) protocol to initiate a calcium microdomain through NMDAR activation at a synapse.
13.  Activity dependent changes in dendritic spine density and spine structure (Crook et al. 2007)
"... In this work, we extend previous modeling studies [27] by combining a model for activity-dependent spine density with one for calcium-mediated spine stem restructuring. ... Additional equations characterize the change in spine density along the dendrite, the current balance equation for an individual spine head, the change in calcium concentration in the spine head, and the dynamics of spine stem resistance. We use computational studies to investigate the changes in spine density and structure for differing synaptic inputs and demonstrate the effects of these changes on the input-output properties of the dendritic branch. ... "
14.  Allen Institute: Gad2-IRES-Cre VISp layer 5 472447460
This is an Allen Cell Types Database model of a Gad2-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
15.  Allen Institute: Gad2-IRES-Cre VISp layer 5 473561729
This is an Allen Cell Types Database model of a Gad2-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
16.  Allen Institute: Htr3a-Cre VISp layer 2/3 472352327
This is an Allen Cell Types Database model of a Htr3a-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
17.  Allen Institute: Htr3a-Cre VISp layer 2/3 472421285
This is an Allen Cell Types Database model of a Htr3a-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
18.  Allen Institute: Nr5a1-Cre VISp layer 2/3 473862496
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
19.  Allen Institute: Nr5a1-Cre VISp layer 4 329322394
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
20.  Allen Institute: Nr5a1-Cre VISp layer 4 472306544
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
21.  Allen Institute: Nr5a1-Cre VISp layer 4 472442377
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
22.  Allen Institute: Nr5a1-Cre VISp layer 4 472451419
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
23.  Allen Institute: Nr5a1-Cre VISp layer 4 472915634
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
24.  Allen Institute: Nr5a1-Cre VISp layer 4 473834758
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
25.  Allen Institute: Nr5a1-Cre VISp layer 4 473863035
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
26.  Allen Institute: Nr5a1-Cre VISp layer 4 473871429
This is an Allen Cell Types Database model of a Nr5a1-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
27.  Allen Institute: Ntsr1-Cre VISp layer 4 472430904
This is an Allen Cell Types Database model of a Ntsr1-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
28.  Allen Institute: Pvalb-IRES-Cre VISp layer 2/3 472306616
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
29.  Allen Institute: Pvalb-IRES-Cre VISp layer 5 471085845
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
30.  Allen Institute: Pvalb-IRES-Cre VISp layer 5 472349114
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
31.  Allen Institute: Pvalb-IRES-Cre VISp layer 5 472912177
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
32.  Allen Institute: Pvalb-IRES-Cre VISp layer 5 473465774
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
33.  Allen Institute: Pvalb-IRES-Cre VISp layer 5 473862421
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
34.  Allen Institute: Pvalb-IRES-Cre VISp layer 6a 471081668
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
35.  Allen Institute: Pvalb-IRES-Cre VISp layer 6a 472301074
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
36.  Allen Institute: Pvalb-IRES-Cre VISp layer 6a 473860269
This is an Allen Cell Types Database model of a Pvalb-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
37.  Allen Institute: Rbp4-Cre VISp layer 5 472424854
This is an Allen Cell Types Database model of a Rbp4-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
38.  Allen Institute: Rbp4-Cre VISp layer 6a 473871592
This is an Allen Cell Types Database model of a Rbp4-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
39.  Allen Institute: Rorb-IRES2-Cre-D VISp layer 2/3 472299294
This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
40.  Allen Institute: Rorb-IRES2-Cre-D VISp layer 2/3 472434498
This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
41.  Allen Institute: Rorb-IRES2-Cre-D VISp layer 4 473863510
This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
42.  Allen Institute: Rorb-IRES2-Cre-D VISp layer 5 471087975
This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
43.  Allen Institute: Rorb-IRES2-Cre-D VISp layer 5 473561660
This is an Allen Cell Types Database model of a Rorb-IRES2-Cre-D neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
44.  Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472300877
This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
45.  Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472427533
This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
46.  Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 472912107
This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
47.  Allen Institute: Scnn1a-Tg2-Cre VISp layer 4 473465456
This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
48.  Allen Institute: Scnn1a-Tg2-Cre VISp layer 5 472306460
This is an Allen Cell Types Database model of a Scnn1a-Tg2-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
49.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 329321704
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
50.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 472363762
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
51.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 473862845
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
52.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 4 473872986
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
53.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 472455509
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
54.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 473863578
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
55.  Allen Institute: Scnn1a-Tg3-Cre VISp layer 5 473871773
This is an Allen Cell Types Database model of a Scnn1a-Tg3-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
56.  Allen Institute: Sst-IRES-Cre VISp layer 2/3 471086533
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
57.  Allen Institute: Sst-IRES-Cre VISp layer 2/3 472304676
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 2/3 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
58.  Allen Institute: Sst-IRES-Cre VISp layer 4 472304539
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 4 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
59.  Allen Institute: Sst-IRES-Cre VISp layer 5 472299363
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
60.  Allen Institute: Sst-IRES-Cre VISp layer 5 472450023
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
61.  Allen Institute: Sst-IRES-Cre VISp layer 5 473835796
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 5 of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
62.  Allen Institute: Sst-IRES-Cre VISp layer 6a 472440759
This is an Allen Cell Types Database model of a Sst-IRES-Cre neuron from layer 6a of the mouse primary visual cortex. The model was based on a traced morphology after filling the cell with biocytin and optimized using experimental electrophysiology data recorded from the same cell. The electrophysiology data was collected in a highly standardized way to facilitate comparison across all cells in the database. The model was optimized by a genetic algorithm that adjusted the densities of conductances placed at the soma to match experimentally-measured features of action potential firing. Data and models from the Allen Cell Types Database are made available to the community under the Allen Institute's Terms of Use and Citation Policy.
63.  BCM-like synaptic plasticity with conductance-based models (Narayanan Johnston, 2010)
" ... Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. ..."
64.  Behavioral time scale synaptic plasticity underlies CA1 place fields (Bittner et al. 2017)
" ... Place fields could be produced in vivo in a single trial by potentiation of input that arrived seconds before and after complex spiking.The potentiated synaptic input was not initially coincident with action potentials or depolarization.This rule, named behavioral timescale synaptic plasticity, abruptly modifies inputs that were neither causal nor close in time to postsynaptic activation. ...", " ... To determine if the above plasticity rule could be observed under more realistic model conditions, we constructed and optimized a biophysically detailed model and attempted to fully account for the experimental data. ... "
65.  Biophysically detailed model of the mouse sino-atrial node cell (Kharche et al. 2011)
This model is developed to study the role of various electrophysiological mechanisms in generating cardiac pacemaking action potentials (APs).The model incorporates membrane ionic currents and intracellular mechanisms contributing to spontaneous mouse SAN APs. The model was validated by testing the functional roles of individual membrane currents in one and multiple parameter analyses.The roles of intracellular Ca2+-handling mechanisms on cardiac pacemaking were also investigated in the model.
66.  Ca(2+) oscillations based on Ca-induced Ca-release (Dupont et al 1991)
We consider a simple, minimal model for signal-induced Ca2+ oscillations based on Ca(2+)-induced Ca2+ release. The model takes into account the existence of two pools of intracellular Ca2+, namely, one sensitive to inositol 1,4,5 trisphosphate (InsP3) whose synthesis is elicited by the stimulus, and one insensitive to InsP3. See paper for more and details.
67.  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. ..."
68.  CA1 pyramidal neuron dendritic spine with plasticity (O`Donnell et al. 2011)
Biophysical model of a dendritic spine and adjacent dendrite with synapse. Model parameters adjusted to fit CA3-CA1 Shaffer collateral synapse data from literature. Model includes both electrical and Ca2+ dynamics, including AMPARs, NMDARs, 4 types of CaV channel, and leak conductance. Spine and synapse are plastic according to Ca2+ dependent rule. The aim of the model is to explore the effects of dendritic spine structural plasticity on the rules of synaptic plasticity.
69.  CA1 pyramidal neuron: dendritic Ca2+ inhibition (Muellner et al. 2015)
In our experimental study, we combined paired patch-clamp recordings and two-photon Ca2+ imaging to quantify inhibition exerted by individual GABAergic contacts on hippocampal pyramidal cell dendrites. We observed that Ca2+ transients from back-propagating action potentials were significantly reduced during simultaneous activation of individual nearby GABAergic synapses. To simulate dendritic Ca2+ inhibition by individual GABAergic synapses, we employed a multi-compartmental CA1 pyramidal cell model with detailed morphology, voltage-gated channel distributions, and calcium dynamics, based with modifications on the model of Poirazi et al., 2003, modelDB accession # 20212.
70.  CA1 pyramidal neuron: Dendritic Na+ spikes are required for LTP at distal synapses (Kim et al 2015)
This model simulates the effects of dendritic sodium spikes initiated in distal apical dendrites on the voltage and the calcium dynamics revealed by calcium imaging. It shows that dendritic sodium spike promotes large and transient calcium influxes via NMDA receptor and L-type voltage-gated calcium channels, which contribute to the induction of LTP at distal synapses.
71.  CA1 pyramidal: Stochastic amplification of KCa in Ca2+ microdomains (Stanley et al. 2011)
This minimal model investigates stochastic amplification of calcium-activated potassium (KCa) currents. Amplification results from calcium being released in short high amplitude pulses associated with the stochastic gating of calcium channels in microdomains. This model predicts that such pulsed release of calcium significantly increases subthreshold SK2 currents above what would be produced by standard deterministic models. However, there is little effect on a simple sAHP current kinetic scheme. This suggests that calcium stochasticity and microdomains should be considered when modeling certain KCa currents near subthreshold conditions.
72.  Ca2+ current versus Ca2+ channel cooperativity of exocytosis (Matveev et al. 2009)
"... While varying extracellular or intracellular Ca2+ concentration assesses the intrinsic biochemical Ca2+ cooperativity of neurotransmitter release, varying the number of open Ca2+ channels using pharmacological channel block or the tail current titration probes the cooperativity between individual Ca2+ channels in triggering exocytosis. ... Here we provide a detailed analysis of the Ca2+ sensitivity measures probed by these experimental protocols, present simple expressions for special cases, and demonstrate the distinction between the Ca2+ current cooperativity, defined by the relationship between exocytosis rate and the whole-terminal Ca2+ current magnitude, and the underlying Ca2+ channel cooperativity, defined as the average number of channels involved in the release of a single vesicle. ... Further, we use three-dimensional computational modeling of buffered Ca2+ diffusion to analyze these distinct Ca2+ cooperativity measures, and demonstrate the role of endogenous Ca2+ buffers on such measures. We show that buffers can either increase or decrease the Ca2+ current cooperativity of exocytosis, depending on their concentration and the single-channel Ca2+ current."
73.  Ca2+ oscillations in single astrocytes (Lavrentovich and Hemkin 2008) (python) (Manninen et al 2017)
We tested the reproducibility and comparability of four astrocyte models (Manninen, Havela, Linne, 2017). Model by Lavrentovich and Hemkin (2008) was one of them. We implemented and ran the model by Lavrentovich and Hemkin (2008) using Jupyter Notebook. Model code produces results of Figure 1 in Manninen, Havela, Linne (2017).
74.  Ca2+ Oscillations in Sympathetic neurons (Friel 1995)
" ... This study focuses on caffeine-induced [Ca2+]i oscillations in sympathetic neurons. ... The aim of the study was to understand the mechanism responsible for the oscillations. As a starting point, [Ca2+]i relaxations were examined after membrane depolarization and exposure to caffeine. For both stimuli, post-stimulus relaxations could be described by the sum of two decaying exponential functions, consistent with a one-pool system in which Ca2+ transport between compartments is regulated by linear Ca2+ pumps and leaks. After modifying the store to include a [Ca2+]i-sensitive leak, the model also exhibits oscillations such as those observed experimentally. ... Thus, a one-pool model with a single [Ca2+]i-sensitive Ca2+ permeability is adequate to account for many of the quantitative properties of steady-state [Ca2+]i oscillations in sympathetic neurons. ..."
75.  Calcium dynamics depend on dendritic diameters (Anwar et al. 2014)
"... in dendrites there is a strong contribution of morphology because the peak calcium levels are strongly determined by the surface to volume ratio (SVR) of each branch, which is inversely related to branch diameter. In this study we explore the predicted variance of dendritic calcium concentrations due to local changes in dendrite diameter and how this is affected by the modeling approach used. We investigate this in a model of dendritic calcium spiking in different reconstructions of cerebellar Purkinje cells and in morphological analysis of neocortical and hippocampal pyramidal neurons. ..."
76.  Calcium influx during striatal upstates (Evans et al. 2013)
"... To investigate the mechanisms that underlie the relationship between calcium and AP timing, we have developed a realistic biophysical model of a medium spiny neuron (MSN). ... Using this model, we found that either the slow inactivation of dendritic sodium channels (NaSI) or the calcium inactivation of voltage-gated calcium channels (CDI) can cause high calcium corresponding to early APs and lower calcium corresponding to later APs. We found that only CDI can account for the experimental observation that sensitivity to AP timing is dependent on NMDA receptors. Additional simulations demonstrated a mechanism by which MSNs can dynamically modulate their sensitivity to AP timing and show that sensitivity to specifically timed pre- and postsynaptic pairings (as in spike timing-dependent plasticity protocols) is altered by the timing of the pairing within the upstate. …"
77.  Calcium response prediction in the striatal spines depending on input timing (Nakano et al. 2013)
We construct an electric compartment model of the striatal medium spiny neuron with a realistic morphology and predict the calcium responses in the synaptic spines with variable timings of the glutamatergic and dopaminergic inputs and the postsynaptic action potentials. The model was validated by reproducing the responses to current inputs and could predict the electric and calcium responses to glutamatergic inputs and back-propagating action potential in the proximal and distal synaptic spines during up and down states.
78.  Calcium spikes in basal dendrites (Kampa and Stuart 2006)
This model was published in Kampa & Stuart (2006) J Neurosci 26(28):7424-32. The simulation creates two plots showing voltage and calcium changes in basal dendrites of layer 5 pyramidal neurons during action potential backpropagation. created by B. Kampa (2006)
79.  Calcium waves and mGluR-dependent synaptic plasticity in CA1 pyr. neurons (Ashhad & Narayanan 2013)
A morphologically realistic, conductance-based model equipped with kinetic schemes that govern several calcium signalling modules and pathways in CA1 pyramidal neurons
80.  Calcium waves in neuroblastoma cells (Fink et al. 2000)
Uses a model of IP3-mediated release of Ca from endoplasmic reticulum (ER) to study how initiation and propagation of Ca waves are affected by cell geometry, spatial distributions of ER and IP3 generation, and diffusion of Ca and mobile buffer.
81.  Cardiac Atrial Cell (Courtemanche et al 1998)
Marc Courtemanche, Rafael J. Ramirez, and Stanley Nattel. Ionic mechanisms underlying human atrial action potential properties insights from a mathematical model Am J Physiol Heart Circ Physiol 1998 275: H301-H321. The implementation of this model in NEURON was contributed by Ingemar Jacobson.
82.  Cardiac sarcomere dynamics (Negroni and Lascano 1996)
"A muscle model establishing the link between cross-bridge dynamics and intracellular Ca2+ kinetics was assessed by simulation of experiments performed in isolated cardiac muscle. The model is composed by the series arrangement of muscle units formed by inextensible thick and thin filaments in parallel with an elastic element. Attached cross-bridges act as independent force generators whose force is linearly related to the elongation of their elastic structure. Ca2+ kinetics is described by a four-state system of sites on the thin filament associated with troponin C: sites with free troponin C (T), sites with Ca2+ bound to troponin C (TCa); sites with Ca2+ bound to troponin C and attached cross-bridges (TCa*); and sites with troponin C not associated with Ca2+ and attached cross-bridges (T*). The intracellular Ca2+ concentration ([Ca2+]) is controlled solely by the sarcoplasmic reticulum through an inflow function and a saturated outflow pump function. ..."
83.  Cerebellar purkinje cell: interacting Kv3 and Na currents influence firing (Akemann, Knopfel 2006)
Purkinje neurons spontaneously generate action potentials in the absence of synaptic drive and thereby exert a tonic, yet plastic, input to their target cells in the deep cerebellar nuclei. Purkinje neurons express two ionic currents with biophysical properties that are specialized for high-frequency firing: resurgent sodium currents and potassium currents mediated by Kv3.3. Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents. See paper for more and details.
84.  Cerebellar purkinje cell: K and Ca channels regulate APs (Miyasho et al 2001)
We adopted De Schutter and Bower's model as the starting point, then modified the descriptions of several ion channels, such as the P-type Ca channel and the delayed rectifier K channel, and added class-E Ca channels and D-type K channels to the model. Our new model reproduces most of our experimental results and supports the conclusions of our experimental study that class-E Ca channels and D-type K channels are present and functioning in the dendrites of Purkinje neurons.
85.  Cerebellum Purkinje cell: dendritic ion channels activated by climbing fibre (Ait Ouares et al 2019)
"In cerebellar Purkinje neuron (PN) dendrites, the transient depolarisation associated with a climbing fibre (CF) EPSP activates voltage-gated Ca2+ channels (VGCCs), voltage-gated K+ channels (VGKCs) and Ca2+ activated SK and BK K+ channels. The resulting membrane potential (Vm) and Ca2+ transients play a fundamental role in dendritic integration and synaptic plasticity of parallel fibre inputs. Here we report a detailed investigation of the kinetics of dendritic Ca2+ and K+ channels activated by CF-EPSPs, based on optical measurements of Vm and Ca2+ transients and on a single-compartment NEURON model reproducing experimental data. ... "
86.  Coincident signals in Olfactory Bulb Granule Cell spines (Aghvami et al 2019)
"In the mammalian olfactory bulb, the inhibitory axonless granule cells (GCs) feature reciprocal synapses that interconnect them with the principal neurons of the bulb, mitral, and tufted cells. These synapses are located within large excitable spines that can generate local action potentials (APs) upon synaptic input (“spine spike”). Moreover, GCs can fire global APs that propagate throughout the dendrite. Strikingly, local postsynaptic Ca2+ entry summates mostly linearly with Ca2+ entry due to coincident global APs generated by glomerular stimulation, although some underlying conductances should be inactivated. We investigated this phenomenon by constructing a compartmental GC model to simulate the pairing of local and global signals as a function of their temporal separation ?t. These simulations yield strongly sublinear summation of spine Ca2+ entry for the case of perfect coincidence ?t = 0 ms. ..."
87.  Computational model of bladder small DRG neuron soma (Mandge & Manchanda 2018)
Bladder small DRG neurons, which are putative nociceptors pivotal to urinary bladder function, express more than a dozen different ionic membrane mechanisms: ion channels, pumps and exchangers. Small-conductance Ca2+-activated K+ (SKCa) channels which were earlier thought to be gated solely by intracellular Ca2+ concentration ([Ca]i ) have recently been shown to exhibit inward rectification with respect to membrane potential. The effect of SKCa inward rectification on the excitability of these neurons is unknown. Furthermore, studies on the role of KCa channels in repetitive firing and their contributions to different types of afterhyperpolarization (AHP) in these neurons are lacking. In order to study these phenomena, we first constructed and validated a biophysically detailed single compartment model of bladder small DRG soma constrained by physiological data. The model includes twenty-two major known membrane mechanisms along with intracellular Ca2+ dynamics comprising Ca2+ diffusion, cytoplasmic buffering, and endoplasmic reticulum (ER) and mitochondrial mechanisms. Using modelling studies, we show that inward rectification of SKCa is an important parameter regulating neuronal repetitive firing and that its absence reduces action potential (AP) firing frequency. We also show that SKCa is more potent in reducing AP spiking than the large-conductance KCa channel (BKCa) in these neurons. Moreover, BKCa was found to contribute to the fast AHP (fAHP) and SKCa to the medium-duration (mAHP) and slow AHP (sAHP). We also report that the slow inactivating A-type K+ channel (slow KA) current in these neurons is composed of 2 components: an initial fast inactivating (time constant ~ 25-100 ms) and a slow inactivating (time constant ~ 200-800 ms) current. We discuss the implications of our findings, and how our detailed model can help further our understanding of the role of C-fibre afferents in the physiology of urinary bladder as well as in certain disorders.
88.  Computer model of clonazepam`s effect in thalamic slice (Lytton 1997)
Demonstration of the effect of a minor pharmacological synaptic change at the network level. Clonazepam, a benzodiazepine, enhances inhibition but is paradoxically useful for certain types of seizures. This simulation shows how inhibition of inhibitory cells (the RE cells) produces this counter-intuitive effect.
89.  Computer simulations of neuron-glia interactions mediated by ion flux (Somjen et al. 2008)
"... To examine the effect of glial K+ uptake, we used a model neuron equipped with Na+, K+, Ca2+ and Cl− conductances, ion pumps and ion exchangers, surrounded by interstitial space and glia. The glial membrane was either “passive”, incorporating only leak channels and an ion exchange pump, or it had rectifying K+ channels. We computed ion fluxes, concentration changes and osmotic volume changes. ... We conclude that voltage gated K+ currents can boost the effectiveness of the glial “potassium buffer” and that this buffer function is important even at moderate or low levels of excitation, but especially so in pathological states."
90.  Conductance based model for short term plasticity at CA3-CA1 synapses (Mukunda & Narayanan 2017)
We develop a new biophysically rooted, physiologically constrained conductance-based synaptic model to mechanistically account for short-term facilitation and depression, respectively through residual calcium and transmitter depletion kinetics. The model exhibits different synaptic filtering profiles upon changing certain parameters in the base model. We show degenercy in achieving similar plasticity profiles with different presynaptic parameters. Finally, by virtually knocking out certain conductances, we show the differential contribution of conductances.
91.  Controlling KCa channels with different Ca2+ buffering models in Purkinje cell (Anwar et al. 2012)
In this work, we compare the dynamics of different buffering models during generation of a dendritic Ca2+ spike in a single compartment model of a Purkinje cell dendrite. The Ca2+ buffering models used are 1) a single Ca2+ pool, 2) two Ca2+ pools respectively for the fast and slow transients, 3) a detailed calcium model with buffers, pump (Schmidt et al., 2003), and diffusion and 4) a calcium model with buffers, pump and diffusion compensation. The parameters of single pool and double pool are tuned, using Neurofitter (Van Geit et al., 2007), to approximate the behavior of detailed calcium dynamics over range of 0.5 µM to 8 µM of intracellular calcium. The diffusion compensation is modeled using a buffer-like mechanism called DCM. To use DCM robustly for different diameter compartments, its parameters are estimated, using Neurofitter (Van Geit et al., 2007), as a function of compartment diameter (0.8 µm-20 µm).
92.  Dendritic signals command firing dynamics in a Cerebellar Purkinje Cell model (Genet et al. 2010)
This model endows the dendrites of a reconstructed Purkinje cells (PC) with the mechanism of Ca-dependent plateau potentials and spikes described in Genet, S., and B. Delord. 2002. A biophysical model of nonlinear dynamics underlying plateau potentials and calcium spikes in Purkinje cell dendrites. J. Neurophysiol. 88:2430–2444). It is a part of a comprehensive mathematical study suggesting that active electric signals in the dendrites of PC command epochs of firing and silencing of the PC soma.
93.  Dendritic spine geometry, spine apparatus organization: spatiotemporal Ca dynamics (Bell et al 2019)
" ... we systematically investigated the relationship between the shape and size of both the spine head and spine apparatus, a specialized endoplasmic reticulum compartment within the spine head, in modulating rapid calcium dynamics using mathematical modeling. ..."
94.  Dentate granule cell: mAHP & sAHP; SK & Kv7/M channels (Mateos-Aparicio et al., 2014)
The model is based on that of Aradi & Holmes (1999; Journal of Computational Neuroscience 6, 215-235). It was used to help understand the contribution of M and SK channels to the medium afterhyperpolarization (mAHP) following one or seven spikes, as well as the contribution of M channels to the slow afterhyperpolarization (sAHP). We found that SK channels are the main determinants of the mAHP, in contrast to CA1 pyramidal cells where the mAHP is primarily caused by the opening of M channels. The model reproduced these experimental results, but we were unable to reproduce the effects of the M-channel blocker XE991 on the sAHP. It is suggested that either the XE991-sensitive component of the sAHP is not due to M channels, or that when contributing to the sAHP, these channels operate in a mode different from that associated with the mAHP.
95.  Dentate gyrus granule cell: calcium and calcium-dependent conductances (Aradi and Holmes 1999)
We have constructed a detailed model of a hippocampal dentate granule (DG) cell that includes nine different channel types. Channel densities and distributions were chosen to reproduce reported physiological responses observed in normal solution and when blockers were applied. The model was used to explore the contribution of each channel type to spiking behavior with particular emphasis on the mechanisms underlying postspike events. ... The model was used to predict changes in channel densities that could lead to epileptogenic burst discharges and to predict the effect of altered buffering capacity on firing behavior. We conclude that the clustered spatial distributions of calcium related channels, the presence of slow delayed rectifier potassium currents in dendrites, and calcium buffering properties, together, might explain the resistance of DG cells to the development of epileptogenic burst discharges.
96.  Determinants of fast calcium dynamics in dendritic spines and dendrites (Cornelisse et al. 2007)
"... Calcium influx time course and calcium extrusion rate were both in the same range for spines and dendrites when fitted with a dynamic multi-compartment model that included calcium binding kinetics and diffusion. In a subsequent analysis we used this model to investigate which parameters are critical determinants in spine calcium dynamics. The model confirmed the experimental findings: a higher SVR (surface-to-volume ratio) is not sufficient by itself to explain the faster rise time kinetics in spines, but only when paired with a lower buffer capacity in spines. Simulations at zero calcium-dye conditions show that calmodulin is more efficiently activated in spines, which indicates that spine morphology and buffering conditions in neocortical spines favor synaptic plasticity. ..."
97.  Deterministic chaos in a mathematical model of a snail neuron (Komendantov and Kononenko 1996)
"Chaotic regimes in a mathematical model of pacemaker activity in the bursting neurons of a snail Helix pomatia, have been investigated. The model includes a slow-wave generating mechanism, a spike-generating mechanism, an inward Ca current, intracellular Ca ions, [Ca2+]in, their fast buffering and uptake by intracellular Ca stores, and a [Ca2+]in-inhibited Ca current. Chemosensitive voltage-activated conductance, gB*, responsible for termination of the spike burst, and chemosensitive sodium conductance, gNa*, responsible for the depolarization phase of the slow-wave, were used as control parameters. ... Time courses of the membrane potential and [Ca2+]in were employed to analyse different regimes in the model. ..."
98.  Differential modulation of pattern and rate in a dopamine neuron model (Canavier and Landry 2006)
"A stylized, symmetric, compartmental model of a dopamine neuron in vivo shows how rate and pattern can be modulated either concurrently or differentially. If two or more parameters in the model are varied concurrently, the baseline firing rate and the extent of bursting become decorrelated, which provides an explanation for the lack of a tight correlation in vivo and is consistent with some independence of the mechanisms that generate baseline firing rates versus bursting. ..." See paper for more and details.
99.  Discrimination on behavioral time-scales mediated by reaction-diffusion in dendrites (Bhalla 2017)
Sequences of events are ubiquitous in sensory, motor, and cognitive function. Key computational operations, including pattern recognition, event prediction, and plasticity, involve neural discrimination of spatio-temporal sequences. Here we show that synaptically-driven reaction diffusion pathways on dendrites can perform sequence discrimination on behaviorally relevant time-scales. We used abstract signaling models to show that selectivity arises when inputs at successive locations are aligned with, and amplified by, propagating chemical waves triggered by previous inputs. We incorporated biological detail using sequential synaptic input onto spines in morphologically, electrically, and chemically detailed pyramidal neuronal models based on rat data.
100.  Disentangling astroglial physiology with a realistic cell model in silico (Savtchenko et al 2018)
"Electrically non-excitable astroglia take up neurotransmitters, buffer extracellular K+ and generate Ca2+ signals that release molecular regulators of neural circuitry. The underlying machinery remains enigmatic, mainly because the sponge-like astrocyte morphology has been difficult to access experimentally or explore theoretically. Here, we systematically incorporate multi-scale, tri-dimensional astroglial architecture into a realistic multi-compartmental cell model, which we constrain by empirical tests and integrate into the NEURON computational biophysical environment. This approach is implemented as a flexible astrocyte-model builder ASTRO. As a proof-of-concept, we explore an in silico astrocyte to evaluate basic cell physiology features inaccessible experimentally. ..."
101.  Endocannabinoid dynamics gate spike-timing dependent depression and potentiation (Cui et al 2016)
The endocannabinoid (eCB) system is considered involved in synaptic depression. Recent reports have also linked eCBs to synaptic potentiation. However it is not known how eCB signaling may support such bidirectionality. To question the mechanisms of this phenomena in spike-timing dependent plasticity (STDP) at corticostriatal synapses, we combined electrophysiology experiments with biophysical modeling. We demonstrate that STDP is controlled by eCB levels and dynamics: prolonged and moderate levels of eCB lead to eCB-mediated long-term depression (eCB-tLTD) while short and large eCB transients produce eCB-mediated long-term potentiation (eCB-tLTP). Therefore, just like neurotransmitters glutamate or GABA, eCB form a bidirectional system.
102.  ERG current in repolarizing plateau potentials in dopamine neurons (Canavier et al 2007)
"Blocking the small-conductance (SK) calcium-activated potassium channel promotes burst firing in dopamine neurons both in vivo and in vitro. ... We focus on the underlying plateau potential oscillation generated in the presence of both apamin and TTX, so that action potentials are not considered. We find that although the plateau potentials are mediated by a voltage-gated Ca2+ current, they do not depend on the accumulation of cytosolic Ca2+, then use a computational model to test the hypothesis that the slowly voltage-activated ether-a-go-go–related gene (ERG) potassium current repolarizes the plateaus. The model, which includes a material balance on calcium, is able to reproduce the time course of both membrane potential and somatic calcium concentration, and can also mimic the induction of plateau potentials by the calcium chelator BAPTA." See paper for more.
103.  Excitability of PFC Basal Dendrites (Acker and Antic 2009)
".. We carried out multi-site voltage-sensitive dye imaging of membrane potential transients from thin basal branches of prefrontal cortical pyramidal neurons before and after application of channel blockers. We found that backpropagating action potentials (bAPs) are predominantly controlled by voltage-gated sodium and A-type potassium channels. In contrast, pharmacologically blocking the delayed rectifier potassium, voltage-gated calcium or Ih, conductance had little effect on dendritic action potential propagation. Optically recorded bAP waveforms were quantified and multicompartmental modeling (NEURON) was used to link the observed behavior with the underlying biophysical properties. The best-fit model included a non-uniform sodium channel distribution with decreasing conductance with distance from the soma, together with a non-uniform (increasing) A-type potassium conductance. AP amplitudes decline with distance in this model, but to a lesser extent than previously thought. We used this model to explore the mechanisms underlying two sets of published data involving high frequency trains of action potentials, and the local generation of sodium spikelets. ..."
104.  Excitation-contraction coupling/mitochondrial energetics (ECME) model (Cortassa et al. 2006)
"An intricate network of reactions is involved in matching energy supply with demand in the heart. This complexity arises because energy production both modulates and is modulated by the electrophysiological and contractile activity of the cardiac myocyte. Here, we present an integrated mathematical model of the cardiac cell that links excitation-contraction coupling with mitochondrial energy generation. The dynamics of the model are described by a system of 50 ordinary differential equations. The formulation explicitly incorporates cytoplasmic ATP-consuming processes associated with force generation and ion transport, as well as the creatine kinase reaction. Changes in the electrical and contractile activity of the myocyte are coupled to mitochondrial energetics through the ATP, Ca21, and Na1 concentrations in the myoplasmic and mitochondrial matrix compartments. ..."
105.  Facilitation model based on bound Ca2+ (Matveev et al. 2006)
"Facilitation is a transient stimulation-induced increase in synaptic response, a ubiquitous form of short-term synaptic plasticity that can regulate synaptic transmission on fast time scales. In their pioneering work, Katz and Miledi and Rahamimoff demonstrated the dependence of facilitation on presynaptic Ca2+ influx and proposed that facilitation results from the accumulation of residual Ca2+ bound to vesicle release triggers. However, this bound Ca2+ hypothesis appears to contradict the evidence that facilitation is reduced by exogenous Ca2+ buffers. This conclusion led to a widely held view that facilitation must depend solely on the accumulation of Ca2+ in free form. Here we consider a more realistic implementation of the bound Ca2+ mechanism, taking into account spatial diffusion of Ca2+, and show that a model with slow Ca2+ unbinding steps can retain sensitivity to free residual Ca2+. ..."
106.  Facilitation through buffer saturation (Matveev et al. 2004)
"... Using computer simulations, we study the magnitude of synaptic facilitation (SF) that can be achieved by a buffer saturation mechanism (BSM), and explore its dependence on the endogenous buffering properties. ..."
107.  Glutamate-evoked Ca2+ oscillations in single astrocytes (De Pitta et al. 2009) (Manninen et al 2017)
We tested the reproducibility and comparability of four astrocyte models (Manninen, Havela, Linne, 2017). Model by De Pitta et al. (2009) was one of them. We implemented and ran the model by De Pitta et al. (2009) using Jupyter Notebook. Model code produces results of Figure 1 and Figures 3-5 in Manninen, Havela, Linne (2017).
108.  Glutamate-evoked Ca2+ oscillations in single astrocytes (Modified from Dupont et al. 2011)
We tested the reproducibility and comparability of four astrocyte models (Manninen, Havela, Linne, 2017). Model by Dupont et al. (2011) was one of them, but we had to modify the model to get more similar results as in the original publication. We implemented and ran the modified model using Jupyter Notebook. Model code produces results of Figure 1 and Figures 3-5 in Manninen, Havela, Linne (2017).
109.  Intrinsic sensory neurons of the gut (Chambers et al. 2014)
A conductance base model of intrinsic neurons neurons in the gastrointestinal tract. The model contains all the major voltage-gated and calcium-gated currents observed in these neurons. This model can reproduce physiological observations such as the response to multiple brief depolarizing currents, prolonged depolarizing currents and hyperpolarizing currents. This model can be used to predict how different currents influence the excitability of intrinsic sensory neurons in the gut.
110.  Ionic current model of a Hypoglossal Motoneuron (Purvis & Butera 2005)
"We have developed a single-compartment, electrophysiological, hypoglossal motoneuron (HM) model based primarily on experimental data from neonatal rat HMs. The model is able to reproduce the fine features of the HM action potential: the fast afterhyperpolarization, the afterdepolarization, and the medium-duration afterhyperpolarization (mAHP). The model also reproduces the repetitive firing properties seen in neonatal HMs and replicates the neuron’s response to pharmacological experiments. The model was used to study the role of specific ionic currents in HM firing and how variations in the densities of these currents may account for age dependent changes in excitability seen in HMs. ..."
111.  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.
112.  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).
113.  Low Threshold Calcium Currents in TC cells (Destexhe et al 1998)
In Destexhe, Neubig, Ulrich, and Huguenard (1998) experiments and models examine low threshold calcium current's (IT, or T-current) distribution in thalamocortical (TC) cells. Multicompartmental modeling supports the hypothesis that IT currents have a density at least several fold higher in the dendrites than the soma. The IT current contributes significantly to rebound bursts and is thought to have important network behavior consequences. See the paper for details. See also http://cns.iaf.cnrs-gif.fr Correspondance may be addressed to Alain Destexhe: Destexhe@iaf.cnrs-gif.fr
114.  Low Threshold Calcium Currents in TC cells (Destexhe et al 1998) (Brian)
R Brette's implementation in Brian 2 of Destexhe et al 1998's model. The author's original code is also available from ModelDB with accession number 279 (yes, was one of the first models in ModelDB)!
115.  Mechanisms of fast rhythmic bursting in a layer 2/3 cortical neuron (Traub et al 2003)
This simulation is based on the reference paper listed below. This port was made by Roger D Traub and Maciej T Lazarewicz (mlazarew at seas.upenn.edu) Thanks to Ashlen P Reid for help with porting a morphology of the cell.
116.  Medial vestibular neuron models (Quadroni and Knopfel 1994)
The structure and the parameters of the model cells were chosen to reproduce the responses of type A and type B MVNns as described in electrophysiological recordings. The emergence of oscillatory firing under these two specific experimental conditions is consistent with electrophysiological recordings not used during construction of the model. We, therefore, suggest that these models have a high predictive value.
117.  Model for K-ATP mediated bursting in mSNc DA neurons (Knowlton et al 2018)
"Burst firing in medial substantia nigra dopamine (mSN DA) neurons has been selectively linked to novelty-induced exploration behavior in mice. Burst firing in mSN DA neurons, in contrast to lateral SN DA neurons, requires functional ATP-sensitive potassium channels (K-ATP) both in vitro and in vivo. However, the precise role of K-ATP channels in promoting burst firing is un-known. We show experimentally that L-type calcium channel activity in mSN DA neurons en-hances open probability of K-ATP channels. We then generated a mathematical model to study the role of Ca2+ dynamics driving K-ATP channel function in mSN DA neurons during bursting. ..."
118.  Model of AngII signaling and membrane electrophysiology (Makadia, Anderson, Fey et al., 2015)
We developed a novel multiscale model to bridge neuropeptide receptor-activated signaling pathway with membrane electrophysiology. The model studies the effects of Angiotensin II (AngII) on neuronal excitability changes mediated by signaling dynamics and downstream phosphorylation of ion channels. The multiscale model was implemented as a set of ordinary differential equations solved using the ode15s solver in Matlab (Mathworks, USA). The signaling reactions were modeled with either mass-action or Michaelis--Menten kinetics and ion channel electrophysiology was modeled according to the Hodgkin-Huxley formalism. These models were initially validated against their respective data domains independently and were integrated to develop a multiscale model of signaling and electrophysiology.
119.  Model of calcium oscillations in olfactory cilia (Reidl et al. 2006)
Simulation of experiments on olfactory receptor neurons (ORNs). Focussing on the negative feedback that calcium (through calmodulin) has on its own influx through CNG channels, this model is able to reproduce both calcium oscillations as well as adaptation behaviour as seen in experiments done with ORNs.
120.  Model of eupnea and sigh generation in respiratory network (Toporikova et al 2015)
Based on recent in vitro data obtained in the mouse embryo, we have built a computational model consisting of two compartments, interconnected through appropriate synapses. One compartment generates sighs and the other produces eupneic bursts. The model reproduces basic features of simultaneous sigh and eupnea generation (two types of bursts differing in terms of shape, amplitude, and frequency of occurrence) and mimics the effect of blocking glycinergic synapses
121.  Modelling platform of the cochlear nucleus and other auditory circuits (Manis & Compagnola 2018)
"Models of the auditory brainstem have been an invaluable tool for testing hypotheses about auditory information processing and for highlighting the most important gaps in the experimental literature. Due to the complexity of the auditory brainstem, and indeed most brain circuits, the dynamic behavior of the system may be difficult to predict without a detailed, biologically realistic computational model. Despite the sensitivity of models to their exact construction and parameters, most prior models of the cochlear nucleus have incorporated only a small subset of the known biological properties. This confounds the interpretation of modelling results and also limits the potential future uses of these models, which require a large effort to develop. To address these issues, we have developed a general purpose, bio-physically detailed model of the cochlear nucleus for use both in testing hypotheses about cochlear nucleus function and also as an input to models of downstream auditory nuclei. The model implements conductance-based Hodgkin-Huxley representations of cells using a Python-based interface to the NEURON simulator. ..."
122.  Multiple dynamical modes of thalamic relay neurons (Wang XJ 1994)
The (Wang 1994) papers model was replicated in python by (Detorakis 2016). "The model is conductance-based and takes advantage of the interplay between a T-type calcium current and a non-specific cation sag current and thus, it is able to generate spindle and delta rhythms." The model also generates intermittent phase locking, non periodic firing, bursts, and tonic spike patterns.
123.  Multiscale simulation of the striatal medium spiny neuron (Mattioni & Le Novere 2013)
"… We present a new event-driven algorithm to synchronize different neuronal models, which decreases computational time and avoids superfluous synchronizations. The algorithm is implemented in the TimeScales framework. We demonstrate its use by simulating a new multiscale model of the Medium Spiny Neuron of the Neostriatum. The model comprises over a thousand dendritic spines, where the electrical model interacts with the respective instances of a biochemical model. Our results show that a multiscale model is able to exhibit changes of synaptic plasticity as a result of the interaction between electrical and biochemical signaling. …"
124.  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. ..."
125.  MyFirstNEURON (Houweling, Sejnowski 1997)
MyFirstNEURON is a NEURON demo by Arthur Houweling and Terry Sejnowski. Perform experiments from the book 'Electrophysiology of the Neuron, A Companion to Shepherd's Neurobiology, An Interactive Tutorial' by John Huguenard & David McCormick, Oxford University Press 1997, or design your own one or two cell simulation.
126.  Neocortical pyramidal neuron: deep; effects of dopamine (Durstewitz et al 2000)
"... Simulated dopamine strongly enhanced high, delay-type activity but not low, spontaneous activity in the model network. Furthermore the strength of an afferent stimulation needed to disrupt delay-type activity increased with the magnitude of the dopamine-induced shifts in network parameters, making the currently active representation much more stable. Stability could be increased by dopamine-induced enhancements of the persistent Na(+) and N-methyl-D-aspartate (NMDA) conductances. Stability also was enhanced by a reduction in AMPA conductances. The increase in GABA(A) conductances that occurs after stimulation of dopaminergic D1 receptors was necessary in this context to prevent uncontrolled, spontaneous switches into high-activity states (i.e., spontaneous activation of task-irrelevant representations). In conclusion, the dopamine-induced changes in the biophysical properties of intrinsic ionic and synaptic conductances conjointly acted to highly increase stability of activated representations in PFC networks and at the same time retain control over network behavior and thus preserve its ability to adequately respond to task-related stimuli. ..." See paper and references for more and details.
127.  Neural mass model of spindle generation in the isolated thalamus (Schellenberger Costa et al. 2016)
The model generates different oscillatory patterns in the thalamus, including delta and spindle band oscillations.
128.  Neural mass model of the sleeping thalamocortical system (Schellenberger Costa et al 2016)
This paper generates typical human EEG data of sleep stages N2/N3 as well as wakefulness and REM sleep.
129.  New and corrected simulations of synaptic facilitation (Matveev et al. 2002)
"A three-dimensional presynaptic calcium diffusion model developed to account for characteristics of transmitter release was modified to provide for binding of calcium to a receptor and subsequent triggering of exocytosis. When low affinity (20 FLM) and rapid kinetics were assumed for the calcium receptor triggering exocytosis, and stimulus parameters were selected to match those of experiments, the simulations predicted a virtual invariance of the time course of transmitter release to paired stimulation, stimulation with pulses of different amplitude, and stimulation in different calcium solutions. ..."
130.  NMDA subunit effects on Calcium and STDP (Evans et al. 2012)
Effect of NMDA subunit on spike timing dependent plasticity.
131.  Nodose sensory neuron (Schild et al. 1994, Schild and Kunze 1997)
This is a simulink implementation of the model described in Schild et al. 1994, and Schild and Kunze 1997 papers on Nodose sensory neurons. These papers describe the sensitivity these models have to their parameters and the match of the models to experimental data.
132.  Nonlinear dendritic processing in barrel cortex spiny stellate neurons (Lavzin et al. 2012)
This is a multi-compartmental simulation of a spiny stellate neuron which is stimulated by a thalamocortical (TC) and cortico-cortical (CC) inputs. No other cells are explicitly modeled; the presynaptic network activation is represented by the number of active synapses. Preferred and non –preferred thalamic directions thus correspond to larder/smaller number of TC synapses. This simulation revealed that randomly activated synapses can cooperatively trigger global NMDA spikes, which involve participation of most of the dendritic tree. Surprisingly, we found that although the voltage profile of the cell was uniform, the calcium influx was restricted to ‘hot spots’ which correspond to synaptic clusters or large conductance synapses
133.  Olfactory bulb mitral cell gap junction NN model: burst firing and synchrony (O`Connor et al. 2012)
In a network of 6 mitral cells connected by gap junction in the apical dendrite tuft, continuous current injections of 0.06 nA are injected into 20 locations in the apical tufts of two of the mitral cells. The current injections into one of the cells starts 10 ms after the other to generate asynchronous firing in the cells (Migliore et al. 2005 protocol). Firing of the cells is asynchronous for the first 120 ms. However after the burst firing phase is completed the firing in all cells becomes synchronous.
134.  Olfactory Bulb mitral-granule network generates beta oscillations (Osinski & Kay 2016)
This model of the dendrodendritic mitral-granule synaptic network generates gamma and beta oscillations as a function of the granule cell excitability, which is represented by the granule cell resting membrane potential.
135.  Paired turbulence and light effect on calcium increase in Hermissenda (Blackwell 2004)
The sea slug Hermissenda learns to associate light and hair cell stimulation, but not when the stimuli are temporally uncorrelated...These issues were addressed using a multi-compartmental computer model of phototransduction, calcium dynamics, and ionic currents of the Hermissenda photoreceptor...simulations show that a potassium leak channel, which closes with an increase in calcium, is required to produce both the untrained LLD and the enhanced LLD due to the decrease in voltage dependent potassium currents.
136.  Pancreatic Beta Cell signalling pathways (Fridlyand & Philipson 2016) (MATLAB)
This is a 3rd party implementation of Fridlyand & Philipson 2016 who's abstract begins "Insulin secretory in pancreatic beta-cells responses to nutrient stimuli and hormonal modulators include multiple messengers and signaling pathways with complex interdependencies. Here we present a computational model that incorporates recent data on glucose metabolism, plasma membrane potential, G-protein-coupled-receptors (GPCR), cytoplasmic and endoplasmic reticulum calcium dynamics, cAMP and phospholipase C pathways that regulate interactions between second messengers in pancreatic beta-cells. The values of key model parameters were inferred from published experimental data. The model gives a reasonable fit to important aspects of experimentally measured metabolic and second messenger concentrations and provides a framework for analyzing the role of metabolic, hormones and neurotransmitters changes on insulin secretion. Our analysis of the dynamic data provides support for the hypothesis that activation of Ca2+-dependent adenylyl cyclases play a critical role in modulating the effects of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and catecholamines. ..."
137.  Paradoxical GABA-mediated excitation (Lewin et al. 2012)
"GABA is the key inhibitory neurotransmitter in the adult central nervous system, but in some circumstances can lead to a paradoxical excitation that has been causally implicated in diverse pathologies from endocrine stress responses to diseases of excitability including neuropathic pain and temporal lobe epilepsy. We undertook a computational modeling approach to determine plausible ionic mechanisms of GABAA-dependent excitation in isolated post-synaptic CA1 hippocampal neurons because it may constitute a trigger for pathological synchronous epileptiform discharge. In particular, the interplay intracellular chloride accumulation via the GABAA receptor and extracellular potassium accumulation via the K/Cl co-transporter KCC2 in promoting GABAA-mediated excitation is complex. ..."
138.  Parallel STEPS: Large scale stochastic spatial reaction-diffusion simulat. (Chen & De Schutter 2017)
" ... In this paper, we describe an MPI-based, parallel operator-splitting implementation for stochastic spatial reaction-diffusion simulations with irregular tetrahedral meshes. The performance of our implementation is first examined and analyzed with simulations of a simple model. We then demonstrate its application to real-world research by simulating the reaction-diffusion components of a published calcium burst model in both Purkinje neuron sub-branch and full dendrite morphologies..."
139.  Persistent Spiking in ACC Neurons (Ratte et al 2018)
"Neurons use action potentials, or spikes, to encode information. Some neurons can store information for short periods (seconds to minutes) by continuing to spike after a stimulus ends, thus enabling working memory. This so-called “persistent” spiking occurs in many brain areas and has been linked to activation of canonical transient receptor potential (TRPC) channels. However, TRPC activation alone is insufficient to explain many aspects of persistent spiking such as resumption of spiking after periods of imposed quiescence. Using experiments and simulations, we show that calcium influx caused by spiking is necessary and sufficient to activate TRPC channels and that the ensuing positive feedback interaction between intracellular calcium and TRPC channel activation can account for many hitherto unexplained aspects of persistent spiking."
140.  Phase plane reveals two slow variables in midbrain dopamine neuron bursts (Yu and Canavier, 2015)
"Midbrain dopamine neurons exhibit a novel type of bursting that we call “inverted square wave bursting” when exposed to Ca2+-activated small conductance (SK) K+ channel blockers in vitro. This type of bursting has three phases: hyperpolarized silence, spiking, and depolarization block. We find that two slow variables are required for this type of bursting, and we show that the three-dimensional bifurcation diagram for inverted square wave bursting is a folded surface with upper (depolarized) and lower (hyperpolarized) branches. ..."
141.  Presynaptic calcium dynamics at neuromuscular junction (Stockbridge, Moore 1984)
The diffusion of calcium is effectively reduced by the ratio of bound to free calcium. Treating the release magnitude as proportional to the fourth power of calcium concentration next to the membrane gives reasonable facilitation with very little release between spikes.
142.  Principles of Computational Modelling in Neuroscience (Book) (Sterratt et al. 2011)
"... This book provides a step-by-step account of how to model the neuron and neural circuitry to understand the nervous system at all levels, from ion channels to networks. Starting with a simple model of the neuron as an electrical circuit, gradually more details are added to include the effects of neuronal morphology, synapses, ion channels and intracellular signaling. The principle of abstraction is explained through chapters on simplifying models, and how simplified models can be used in networks. This theme is continued in a final chapter on modeling the development of the nervous system. Requiring an elementary background in neuroscience and some high school mathematics, this textbook is an ideal basis for a course on computational neuroscience."
143.  Pyramidal neuron conductances state and STDP (Delgado et al. 2010)
Neocortical neurons in vivo process each of their individual inputs in the context of ongoing synaptic background activity, produced by the thousands of presynaptic partners a typical neuron has. That background activity affects multiple aspects of neuronal and network function. However, its effect on the induction of spike-timing dependent plasticity (STDP) is not clear. Using the present biophysically-detailed computational model, it is not only able to replicate the conductance-dependent shunting of dendritic potentials (Delgado et al,2010), but show that synaptic background can truncate calcium dynamics within dendritic spines, in a way that affects potentiation more strongly than depression. This program uses a simplified layer 2/3 pyramidal neuron constructed in NEURON. It was similar to the model of Traub et al., J Neurophysiol. (2003), and consisted of a soma, an apical shaft, distal dendrites, five basal dendrites, an axon, and a single spine. The spine’s location was variable along the apical shaft (initial 50 μm) and apical. The axon contained an axon hillock region, an initial segment, segments with myelin, and nodes of Ranvier, in order to have realistic action potential generation. For more information about the model see supplemental material, Delgado et al 2010.
144.  Pyramidal Neuron: Deep, Thalamic Relay and Reticular, Interneuron (Destexhe et al 1998, 2001)
This package shows single-compartment models of different classes of cortical neurons, such as the "regular-spiking", "fast-spiking" and "bursting" (LTS) neurons. The mechanisms included are the Na+ and K+ currents for generating action potentials (INa, IKd), the T-type calcium current (ICaT), and a slow voltage-dependent K+ current (IM). See http://cns.fmed.ulaval.ca/alain_demos.html
145.  Quantal neurotransmitter release kinetics with fixed and mobile Ca2+ buffers (Gilmanov et al. 2008)
"... In this work, we used computer modeling of quanta release kinetics with various levels of calcium influx and in the presence of endogenous calcium buffers with varying mobilities. The results of this modeling revealed the desynchronization of quanta release under low calcium influx in the presence of an endogenous fixed calcium buffer, with a diffusion coefficient much smaller than that of free Ca2+, and synchronization occurred upon adding a mobile buffer. This corresponds to changes in secretion time course parameters found experimentally ..."
146.  Rat LGN Thalamocortical Neuron (Connelly et al 2015, 2016)
" ... Here, combining data from fluorescence-targeted dendritic recordings and Ca2+ imaging from low-threshold spiking cells in rat brain slices with computational modeling, the cellular mechanism responsible for LTS (Low Threshold Spike) generation is established. ..." " ... Using dendritic recording, 2-photon glutamate uncaging, and computational modeling, we investigated how rat dorsal lateral geniculate nucleus thalamocortical neurons integrate excitatory corticothalamic feedback. ..."
147.  Reciprocal regulation of rod and cone synapse by NO (Kourennyi et al 2004)
We constructed models of rod and cone photoreceptors using NEURON software to predict how changes in Ca channels would affect the light response in these cells and in postsynaptic horizontal cells.
148.  Reproducibility and comparability of models for astrocyte Ca2+ excitability (Manninen et al 2017)
We tested the reproducibility and comparability of four astrocyte models (Manninen, Havela, Linne, 2017). We implemented and ran the python models using Jupyter Notebook. Model code produces results of Figure 1 and Figures 3-5 and partly Figure 2 in Manninen, Havela, Linne (2017).
149.  Ribbon Synapse (Sikora et al 2005)
A model of the ribbon synapse was developed to replicate both pre- and postsynaptic functions of this glutamatergic juncture. The presynaptic portion of the model is rich in anatomical and physiological detail and includes multiple release sites for each ribbon based on anatomical studies of presynaptic terminals, presynaptic voltage at the terminal, the activation of voltage-gated calcium channels and a calcium-dependent release mechanism whose rate varies as a function of the calcium concentration that is monitored at two different sites which control both an ultrafast, docked pool of vesicles and a release ready pool of tethered vesicles. See paper for more and details.
150.  Rod photoreceptor (Barnes and Hille 1989, Publio et al. 2006, Kourennyi and Liu et al. 2004)
This a conductance-based model of a rod photoreceptor cell based on other modeling works (Barnes and Hille 1989 and Publio et al. 2006 and Kourennyi and Liu et al. 2004 ). In this model four types of ionic channels identified in the inner segment of the rod: nonselective cation channel (h), delayed rectifying potassium channel (Kv), noninactivating potassium channel (Kx) and calcium channel (Ca) was used. The model accurately reproduces the rod response when stimulated with a simulated photocurrent signal. We can show the effect of nonselective cation channel. The absence of this channel cause increasing the peak amplitude and the time to reach the peak of voltage response and absence of transient mode in this response.
151.  Salamander retinal ganglian cells: morphology influences firing (Sheasby, Fohlmeister 1999)
Nerve impulse entrainment and other excitation and passive phenomena are analyzed for a morphologically diverse and exhaustive data set (n=57) of realistic (3-dimensional computer traced) soma-dendritic tree structures of ganglion cells in the tiger salamander (Ambystoma tigrinum) retina.
152.  Salamander retinal ganglion cell: ion channels (Fohlmeister, Miller 1997)
A realistic five (5) channel spiking model reproduces the bursting behavior of tiger salamander ganglion cells in the retina. Please see the readme for more information.
153.  Simulated light response in rod photoreceptors (Liu and Kourennyi 2004)
We developed a complete computer model of the rod, which accurately reproduced the main features of the light response and allowed us to demonstrate that it was suppression of Kx channels that was essential for slowing SLR and increasing excitability of rods. The results reported in this work further establish the importance of Kx channels in rod photoreceptor function.
154.  Simulation of calcium signaling in fine astrocytic processes (Denizot et al 2019)
This model corresponds to the model presented in Denizot et al, 2019. The model indicates that the frequency of calcium signals crucially depends on the spatial organization of the IP3R channels, including their clustering and co-localization with the other sources of calcium influx to the cytosol. Spontaneous calcium signals generated by the model with realistic PAPs volume and calcium concentration successfully reproduce spontaneous calcium transients that we measured in calcium micro-domains with confocal microscopy. To our knowledge, this model is the first model suited to the investigation of spontaneous calcium dynamics in fine astrocytic processes, a crucial step towards a better understanding of the spatio-temporal integration of astrocyte signals in response to neuronal activity.
155.  Species-specific wiring for direction selectivity in the mammalian retina (Ding et al 2016)
" ... Here we present a detailed connectomic reconstruction of SAC circuitry in mouse retina and describe two previously unknown features of synapse distributions along SAC dendrites: input and output synapses are segregated, with inputs restricted to proximal dendrites; and the distribution of inhibitory inputs is fundamentally different from that observed in rabbit retina. An anatomically constrained SAC network model suggests that SAC–SAC wiring differences between mouse and rabbit retina underlie distinct contributions of synaptic inhibition to velocity and contrast tuning and receptive field structure. In particular, the model indicates that mouse connectivity enables SACs to encode lower linear velocities that account for smaller eye diameter, thereby conserving angular velocity tuning. These predictions are confirmed with calcium imaging of mouse SAC dendrites responding to directional stimuli. ..."
156.  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.
157.  Spine neck plasticity controls postsynaptic calcium signals (Grunditz et al. 2008)
This model was set up to dissect the relative contribution of different channels to the spine calcium transients measured at single spines.
158.  Spontaneous calcium oscillations in astrocytes (Lavrentovich and Hemkin 2008)
" ... We propose here a mathematical model of how spontaneous Ca2+ oscillations arise in astrocytes. This model uses the calcium-induced calcium release and inositol cross-coupling mechanisms coupled with a receptor-independent method for producing inositol (1,4,5)-trisphosphate as the heart of the model. By computationally mimicking experimental constraints we have found that this model provides results that are qualitatively similar to experiment."
159.  Spontaneous calcium oscillations in single astrocytes (Riera et al. 2011) (Manninen et al 2017)
We tested the reproducibility and comparability of four astrocyte models (Manninen, Havela, Linne, 2017). Model by Riera et al. (2011) was one of them. We implemented and ran the model by Riera et al. (2011) using Jupyter Notebook. Model codes produce results of Figures 1 and 2 in Manninen, Havela, Linne (2017).
160.  State dependent drug binding to sodium channels in the dentate gyrus (Thomas & Petrou 2013)
A Markov model of sodium channels was developed that includes drug binding to fast inactivated states. This was incorporated into a model of the dentate gyrus to investigate the effects of anti-epileptic drugs on neuron and network properties.
161.  STDP depends on dendritic synapse location (Letzkus et al. 2006)
This model was published in Letzkus, Kampa & Stuart (2006) J Neurosci 26(41):10420-9. The simulation creates several plots showing voltage and NMDA current and conductance changes at different apical dendritic locations in layer 5 pyramidal neurons during STDP induction protocols. Created by B. Kampa (2006).
162.  Stochastic automata network Markov model descriptors of coupled Ca2+ channels (Nguyen et al. 2005)
"... Here we present a formalism by which mathematical models for Ca2+-regulated Ca2+ release sites are derived from stochastic models of single-channel gating that include Ca2+ activation, Ca2+ inactivation, or both. Such models are stochastic automata networks (SANs) that involve a large number of functional transitions, that is, the transition probabilities of the infinitesimal generator matrix of one of the automata (i.e., an individual channel) may depend on the local [Ca2+] and thus the state of the other channels. Simulation and analysis of the SAN descriptors representing homogeneous clusters of intracellular Ca2+ channels show that (1) release site density can modify both the steady-state open probability and stochastic excitability of Ca2+ release sites, (2) Ca2+ inactivation is not a requirement for Ca2+ puffs or sparks, and (3) a single-channel model with a bell-shaped open probability curve does not lead to release site activity that is a biphasic function of release site density. ..."
163.  Stochastic calcium mechanisms cause dendritic calcium spike variability (Anwar et al. 2013)
" ... In single Purkinje cells, spontaneous and synaptically evoked dendritic calcium bursts come in a variety of shapes with a variable number of spikes. The mechanisms causing this variability have never been investigated thoroughly. In this study, a detailed computational model employing novel simulation routines is applied to identify the roles that stochastic ion channels, spatial arrangements of ion channels and stochastic intracellular calcium have towards producing calcium burst variability. … Our findings suggest that stochastic intracellular calcium mechanisms play a crucial role in dendritic calcium spike generation and are, therefore, an essential consideration in studies of neuronal excitability and plasticity."
164.  Stochastic model of the olfactory cilium transduction and adaptation (Antunes et al 2014)
" ... In this work, we have combined stochastic computational modeling and a systematic pharmacological study of different signaling pathways to investigate their impact during short-term adaptation (STA). ... These results suggest that G-coupled receptors (GPCRs) cycling is involved with the occurrence of STA. To gain insights on the dynamical aspects of this process, we developed a stochastic computational model. The model consists of the olfactory transduction currents mediated by the cyclic nucleotide gated (CNG) channels and calcium ion (Ca2+)-activated chloride (CAC) channels, and the dynamics of their respective ligands, cAMP and Ca2+, and it simulates the EOG (electroolfactogram) results obtained under different experimental conditions through changes in the amplitude and duration of cAMP and Ca2+ response, two second messengers implicated with STA occurrence. The model reproduced the experimental data for each pharmacological treatment and provided a mechanistic explanation for the action of GPCR cycling in the levels of second messengers modulating the levels of STA. All together, these experimental and theoretical results indicate the existence of a mechanism of regulation of STA by signaling pathways that control GPCR cycling and tune the levels of second messengers in OSNs, and not only by CNG channel desensitization as previously thought. "
165.  Striatal Spiny Projection Neuron (SPN) plasticity rule (Jedrzejewska-Szmek et al 2016)
166.  Striatal Spiny Projection Neuron, inhibition enhances spatial specificity (Dorman et al 2018)
We use a computational model of a striatal spiny projection neuron to investigate dendritic spine calcium dynamics in response to spatiotemporal patterns of synaptic inputs. We show that spine calcium elevation is stimulus-specific, with supralinear calcium elevation in cooperatively stimulated spines. Intermediate calcium elevation occurs in neighboring non-stimulated dendritic spines, predicting heterosynaptic effects. Inhibitory synaptic inputs enhance the difference between peak calcium in stimulated spines, and peak calcium in non-stimulated spines, thereby enhancing stimulus specificity.
167.  Synaptic integration in a model of granule cells (Gabbiani et al 1994)
We have developed a compartmental model of a turtle cerebellar granule cell consisting of 13 compartments that represent the soma and 4 dendrites. We used this model to investigate the synaptic integration of mossy fiber inputs in granule cells. See reference or abstract at PubMed link below for more information.
168.  Temporal decorrelation by intrinsic cellular dynamics (Wang et al 2003)
"... Recent investigations in primary visual (V1) cortical neurons have demonstrated that adaptation to prolonged changes in stimulus contrast is mediated in part through intrinsic ionic currents, a Ca2+ activated K+ current (IKCa) and especially a Na+ activated K+ current (IKNa). The present study was designed to test the hypothesis that the activation of adaptation ionic currents may provide a cellular mechanism for temporal decorrelation in V1. A conductance-based neuron model was simulated, which included an IKCa and an IKNa. We show that the model neuron reproduces the adaptive behavior of V1 neurons in response to high contrast inputs. ...". See paper for details and more.
169.  Thalamic quiescence of spike and wave seizures (Lytton et al 1997)
A phase plane analysis of a two cell interaction between a thalamocortical neuron (TC) and a thalamic reticularis neuron (RE).
170.  Thalamic Reticular Network (Destexhe et al 1994)
Demo for simulating networks of thalamic reticular neurons (reproduces figures from Destexhe A et al 1994)
171.  Thalamic reticular neurons: the role of Ca currents (Destexhe et al 1996)
The experiments and modeling reported in this paper show how intrinsic bursting properties of RE cells may be explained by dendritic calcium currents.
172.  Thalamocortical and Thalamic Reticular Network (Destexhe et al 1996)
NEURON model of oscillations in networks of thalamocortical and thalamic reticular neurons in the ferret. (more applications for a model quantitatively identical to previous DLGN model; updated for NEURON v4 and above)
173.  Theta phase precession in a model CA3 place cell (Baker and Olds 2007)
"... The present study concerns a neurobiologically based computational model of the emergence of theta phase precession in which the responses of a single model CA3 pyramidal cell are examined in the context of stimulation by realistic afferent spike trains including those of place cells in entorhinal cortex, dentate gyrus, and other CA3 pyramidal cells. Spike-timing dependent plasticity in the model CA3 pyramidal cell leads to a spatially correlated associational synaptic drive that subsequently creates a spatially asymmetric expansion of the model cell’s place field. ... Through selective manipulations of the model it is possible to decompose theta phase precession in CA3 into the separate contributing factors of inheritance from upstream afferents in the dentate gyrus and entorhinal cortex, the interaction of synaptically controlled increasing afferent drive with phasic inhibition, and the theta phase difference between dentate gyrus granule cell and CA3 pyramidal cell activity."
174.  Tonic activation of extrasynaptic NMDA-R promotes bistability (Gall & Dupont 2020)
Our theoretical model provides a simple description of neuronal electrical activity that takes into account the tonic activity of extrasynaptic NMDA receptors and a cytosolic calcium compartment. We show that calcium influx mediated by the tonic activity of NMDA-R can be coupled directly to the activation of calcium-activated potassium channels, resulting in an overall inhibitory effect on neuronal excitability. Furthermore, the presence of tonic NMDA-R activity promotes bistability in electrical activity by dramatically increasing the stimulus interval where both a stable steady state and repetitive firing can coexist. These results could provide an intrinsic mechanism for the constitution of memory traces in neuronal circuits.
175.  Tonic neuron in spinal lamina I: prolongation of subthreshold depol. (Prescott and De Koninck 2005)
Model demonstrates mechanism whereby two kinetically distinct inward currents act synergistically to prolong subthreshold depolarization. The important currents are a persistent Na current (with fast kinetics) and a persistent Ca current (with slower kinetics). Model also includes a slow K current and transient Ca current, in addition to standard HH currents. Model parameters are set to values used in Fig. 8A. Simulation shows prolonged depolarizations in response to two brief stimuli.
176.  Transmitter release and Ca diffusion models (Yamada and Zucker 1992)
"A three-dimensional presynaptic calcium diffusion model developed to account for characteristics of transmitter release was modified to provide for binding of calcium to a receptor and subsequent triggering of exocytosis. ..."
177.  Ventricular cell model (Luo Rudy dynamic model) (Luo Rudy 1994) used in (Wang et al 2006) (XPP)
A mathematical model of the membrane action potential of the mammalian ventricular cell introduced in Luo, Rudy 1991 and used in Wang et al 2006 is made available here in XPP. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. ... The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics. See papers for more and details.

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