Inhibitory Regulation of Excitatory Neurotransmission [electronic resource] / edited by Mark G. Darlison.
Tipo de material: TextoSeries Results and Problems in Cell Differentiation ; 44 | Results and Problems in Cell Differentiation ; 44Editor: Berlin, Heidelberg : Springer Berlin Heidelberg, 2008Descripción: XVI, 248 p. online resourceTipo de contenido:- text
- computer
- online resource
- 9783540726029
- SpringerLink (Online service)
- 573.8 23
- QP351-495
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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