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Inhibitory Regulation of Excitatory Neurotransmission [electronic resource] / edited by Mark G. Darlison.

Contributor(s): Series: Results and Problems in Cell Differentiation ; 44Publisher: Berlin, Heidelberg : Springer Berlin Heidelberg, 2008Description: XVI, 248 p. online resourceContent type:
  • text
Media type:
  • computer
Carrier type:
  • online resource
ISBN:
  • 9783540726029
Subject(s): Genre/Form: Additional physical formats: Printed edition:: No titleDDC classification:
  • 573.8 23
LOC classification:
  • QP351-495
Online resources:
Contents:
Regulation of Excitation by GABAA Receptor Internalization -- Regulation of Excitability by Extrasynaptic GABAA Receptors -- GABAC Receptors in Retina and Brain -- Presynaptic Ionotropic GABA Receptors -- The Role of GABAB Receptors in the Regulation of Excitatory Neurotransmission -- GABAergic Control of CA3-driven Network Events in the Developing Hippocampus -- Regulation of Excitation by Glycine Receptors -- Regulation of Excitability by Potassium Channels -- Modulation of Excitation by Metabotropic Glutamate Receptors -- Presynaptic Inhibition of Glutamate Release by Neuropeptides: Use-Dependent Synaptic Modification -- Regulation of Excitation by GABA Neurotransmission: Focus on Metabolism and Transport -- Human Disorders Caused by the Disruption of the Regulation of Excitatory Neurotransmission.
In: Springer eBooksSummary: Within the central and peripheral nervous systems of animals, including man, inhibition is crucial to counterbalance excitatory neurotransmission, which is predominantly mediated by glutamate and its receptors. Although, particularly in brain, much of this inhibition is provided by classical post-synaptic GABAA receptors, many other proteins and mechanisms regulate excitation. These exist both to "fine tune" neurotransmission and to prevent overexcitation that could lead to conditions such as epilepsy and excitotoxicity, which can result in cell death. This book reviews aspects of GABAA receptor function, as well as the properties of a variety of other important inhibitory proteins, such as GABAC receptors, G-protein coupled receptors (specifically, GABAB receptors, metabotropic glutamate receptors and neuropeptide receptors), glycine receptors, GABA transporters and potassium channels. In addition, the consequences of mutations that disrupt the regulation of excitatory neurotransmission, and efforts to target the GABAergic system for therapeutic benefit, are discussed.
Item type: eBooks
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Regulation of Excitation by GABAA Receptor Internalization -- Regulation of Excitability by Extrasynaptic GABAA Receptors -- GABAC Receptors in Retina and Brain -- Presynaptic Ionotropic GABA Receptors -- The Role of GABAB Receptors in the Regulation of Excitatory Neurotransmission -- GABAergic Control of CA3-driven Network Events in the Developing Hippocampus -- Regulation of Excitation by Glycine Receptors -- Regulation of Excitability by Potassium Channels -- Modulation of Excitation by Metabotropic Glutamate Receptors -- Presynaptic Inhibition of Glutamate Release by Neuropeptides: Use-Dependent Synaptic Modification -- Regulation of Excitation by GABA Neurotransmission: Focus on Metabolism and Transport -- Human Disorders Caused by the Disruption of the Regulation of Excitatory Neurotransmission.

Within the central and peripheral nervous systems of animals, including man, inhibition is crucial to counterbalance excitatory neurotransmission, which is predominantly mediated by glutamate and its receptors. Although, particularly in brain, much of this inhibition is provided by classical post-synaptic GABAA receptors, many other proteins and mechanisms regulate excitation. These exist both to "fine tune" neurotransmission and to prevent overexcitation that could lead to conditions such as epilepsy and excitotoxicity, which can result in cell death. This book reviews aspects of GABAA receptor function, as well as the properties of a variety of other important inhibitory proteins, such as GABAC receptors, G-protein coupled receptors (specifically, GABAB receptors, metabotropic glutamate receptors and neuropeptide receptors), glycine receptors, GABA transporters and potassium channels. In addition, the consequences of mutations that disrupt the regulation of excitatory neurotransmission, and efforts to target the GABAergic system for therapeutic benefit, are discussed.

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