Implementing the cellular mechanisms of synaptic transmission in a neural mass model of the thalamo-cortical circuitryCitation formats

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  • Basabdatta S Bhattacharya

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Implementing the cellular mechanisms of synaptic transmission in a neural mass model of the thalamo-cortical circuitry. / Bhattacharya, Basabdatta S.

In: Frontiers in Computational Neuroscience, Vol. 7, 2013, p. 81.

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Bhattacharya, Basabdatta S. / Implementing the cellular mechanisms of synaptic transmission in a neural mass model of the thalamo-cortical circuitry. In: Frontiers in Computational Neuroscience. 2013 ; Vol. 7. pp. 81.

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@article{7b31313299ae4637abf519e9cf12bb14,
title = "Implementing the cellular mechanisms of synaptic transmission in a neural mass model of the thalamo-cortical circuitry",
abstract = "A novel direction to existing neural mass modeling technique is proposed where the commonly used {"}alpha function{"} for representing synaptic transmission is replaced by a kinetic framework of neurotransmitter and receptor dynamics. The aim is to underpin neuro-transmission dynamics associated with abnormal brain rhythms commonly observed in neurological and psychiatric disorders. An existing thalamocortical neural mass model is modified by using the kinetic framework for modeling synaptic transmission mediated by glutamatergic and GABA (gamma-aminobutyric-acid)-ergic receptors. The model output is compared qualitatively with existing literature on in vitro experimental studies of ferret thalamic slices, as well as on single-neuron-level model based studies of neuro-receptor and transmitter dynamics in the thalamocortical tissue. The results are consistent with these studies: the activation of ligand-gated GABA receptors is essential for generation of spindle waves in the model, while blocking this pathway leads to low-frequency synchronized oscillations such as observed in slow-wave sleep; the frequency of spindle oscillations increase with increased levels of post-synaptic membrane conductance for AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid) receptors, and blocking this pathway effects a quiescent model output. In terms of computational efficiency, the simulation time is improved by a factor of 10 compared to a similar neural mass model based on alpha functions. This implies a dramatic improvement in computational resources for large-scale network simulation using this model. Thus, the model provides a platform for correlating high-level brain oscillatory activity with low-level synaptic attributes, and makes a significant contribution toward advancements in current neural mass modeling paradigm as a potential computational tool to better the understanding of brain oscillations in sickness and in health.",
keywords = "Journal Article",
author = "Bhattacharya, {Basabdatta S}",
year = "2013",
doi = "10.3389/fncom.2013.00081",
language = "English",
volume = "7",
pages = "81",
journal = "Frontiers in Computational Neuroscience",
issn = "1662-5188",
publisher = "Frontiers Media S. A.",

}

RIS

TY - JOUR

T1 - Implementing the cellular mechanisms of synaptic transmission in a neural mass model of the thalamo-cortical circuitry

AU - Bhattacharya, Basabdatta S

PY - 2013

Y1 - 2013

N2 - A novel direction to existing neural mass modeling technique is proposed where the commonly used "alpha function" for representing synaptic transmission is replaced by a kinetic framework of neurotransmitter and receptor dynamics. The aim is to underpin neuro-transmission dynamics associated with abnormal brain rhythms commonly observed in neurological and psychiatric disorders. An existing thalamocortical neural mass model is modified by using the kinetic framework for modeling synaptic transmission mediated by glutamatergic and GABA (gamma-aminobutyric-acid)-ergic receptors. The model output is compared qualitatively with existing literature on in vitro experimental studies of ferret thalamic slices, as well as on single-neuron-level model based studies of neuro-receptor and transmitter dynamics in the thalamocortical tissue. The results are consistent with these studies: the activation of ligand-gated GABA receptors is essential for generation of spindle waves in the model, while blocking this pathway leads to low-frequency synchronized oscillations such as observed in slow-wave sleep; the frequency of spindle oscillations increase with increased levels of post-synaptic membrane conductance for AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid) receptors, and blocking this pathway effects a quiescent model output. In terms of computational efficiency, the simulation time is improved by a factor of 10 compared to a similar neural mass model based on alpha functions. This implies a dramatic improvement in computational resources for large-scale network simulation using this model. Thus, the model provides a platform for correlating high-level brain oscillatory activity with low-level synaptic attributes, and makes a significant contribution toward advancements in current neural mass modeling paradigm as a potential computational tool to better the understanding of brain oscillations in sickness and in health.

AB - A novel direction to existing neural mass modeling technique is proposed where the commonly used "alpha function" for representing synaptic transmission is replaced by a kinetic framework of neurotransmitter and receptor dynamics. The aim is to underpin neuro-transmission dynamics associated with abnormal brain rhythms commonly observed in neurological and psychiatric disorders. An existing thalamocortical neural mass model is modified by using the kinetic framework for modeling synaptic transmission mediated by glutamatergic and GABA (gamma-aminobutyric-acid)-ergic receptors. The model output is compared qualitatively with existing literature on in vitro experimental studies of ferret thalamic slices, as well as on single-neuron-level model based studies of neuro-receptor and transmitter dynamics in the thalamocortical tissue. The results are consistent with these studies: the activation of ligand-gated GABA receptors is essential for generation of spindle waves in the model, while blocking this pathway leads to low-frequency synchronized oscillations such as observed in slow-wave sleep; the frequency of spindle oscillations increase with increased levels of post-synaptic membrane conductance for AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid) receptors, and blocking this pathway effects a quiescent model output. In terms of computational efficiency, the simulation time is improved by a factor of 10 compared to a similar neural mass model based on alpha functions. This implies a dramatic improvement in computational resources for large-scale network simulation using this model. Thus, the model provides a platform for correlating high-level brain oscillatory activity with low-level synaptic attributes, and makes a significant contribution toward advancements in current neural mass modeling paradigm as a potential computational tool to better the understanding of brain oscillations in sickness and in health.

KW - Journal Article

U2 - 10.3389/fncom.2013.00081

DO - 10.3389/fncom.2013.00081

M3 - Article

C2 - 23847522

VL - 7

SP - 81

JO - Frontiers in Computational Neuroscience

JF - Frontiers in Computational Neuroscience

SN - 1662-5188

ER -