Inhibitory Regulation of Excitatory Neurotransmission

Inhibitory Regulation of Excitatory Neurotransmission

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in Vorbereitung

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.



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.
ISBN 978-3-540-72601-2
Artikelnummer 9783540726012
Medientyp Buch
Copyrightjahr 2007
Verlag Springer, Berlin
Umfang XVI, 248 Seiten
Abbildungen XVI, 248 p.
Sprache Englisch