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Modulation of Presynaptic Calcium Channels (Record no. 18919)

000 -LEADER
fixed length control field 04722nam a22004575i 4500
003 - CONTROL NUMBER IDENTIFIER
control field OSt
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20140310150254.0
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION
fixed length control field cr nn 008mamaa
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 130424s2013 ne | s |||| 0|eng d
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9789400763340
978-94-007-6334-0
050 #4 - LIBRARY OF CONGRESS CALL NUMBER
Classification number R-RZ
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 610
Edition number 23
264 #1 -
-- Dordrecht :
-- Springer Netherlands :
-- Imprint: Springer,
-- 2013.
912 ## -
-- ZDB-2-SBL
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Stephens, Gary.
Relator term editor.
245 10 - IMMEDIATE SOURCE OF ACQUISITION NOTE
Title Modulation of Presynaptic Calcium Channels
Medium [electronic resource] /
Statement of responsibility, etc edited by Gary Stephens, Sumiko Mochida.
300 ## - PHYSICAL DESCRIPTION
Extent XII, 365 p. 49 illus., 38 illus. in color.
Other physical details online resource.
505 0# - FORMATTED CONTENTS NOTE
Formatted contents note Spatial and temporal regulation of Ca2+ channels -- Neuronal functions of auxiliary calcium channel subunits.- Reciprocal regulation of neuronal calcium channels by synaptic proteins -- Molecular architecture of Ca2+ channel complexes organized by β subunits in presynaptic active zones -- Control of CaV2 calcium channels and neurosecretion by heterotrimeric G protein coupled receptors -- Regulation of CaV2 channels by small GTPases -- Protein interaction partners of Cav2.3 R-type voltage-gated calcium channels -- Voltage-gated calcium channel signaling to the nucleus -- Presynaptic Ca2+ influx and its modulation at auditory calyceal terminals -- Use of synthetic Ca2+ channel peptides to study presynaptic function -- Impact of a loss-of-function P/Q type Ca2+ channel mutation on excitatory synaptic control of cerebellar Purkinje neurons -- CaV2.1 (P/Q) voltage activated Ca2+ channels and synaptic transmission in genetic and autoimmune diseases -- Splicing and editing to customize CaV channel structures for optimal neural function -- Presynaptic calcium channels as drug targets for pain -- Sensory pathway modulation by calcium channel a2d1 subunit.
520 ## - SUMMARY, ETC.
Summary, etc This book brings together leading international experts to discuss recent advances in the regulation of presynaptic voltage-gated Ca2+ channels (VGCCs), key signal transducers that represent one of the most widely modulated proteins in the body. It is now commonly accepted that presence of the VGCC complex defines an excitable cell. At a basic level, VGCCs transduce membrane potential change to chemical neurotransmitter release at presynaptic terminals. However, on-going scientific research, presented here, in areas including neuroscience, electrophysiology, pharmacology, biochemistry and, increasingly, proteomics, has revealed the widespread nature of modulation of the presynaptic VGCC complex. This book reviews and discusses the following topics: The fundamental role of the VGCC pore-forming CaVa subunit, and some of their binding partners, in presynaptic function and synaptic plasticity. Modulation of presynaptic CaVa subunits by auxiliary CaVb and a2d subunits and by their major interaction partners, such as active zone scaffolding proteins, synaptic proteins, G proteins and small GTPases, which, together, contribute to the VGCC proteome. Work at the cutting edge of research, including how direct electrophysiology recordings from presynaptic terminals and introduction of synthetic CaVa peptides into presynaptic terminals has expanded our knowledge of VGCC function. Evidence emerging over the last decade demonstrating that VGCC subunits represent bona fide molecular targets for therapeutic drug discovery. This development is illustrated by the introduction of the CaV2.2 blocker ziconotide, which represents an important proof-of-concept, but is best exemplified by the emergence of gabapentinoids, which bind the VGCC auxiliary a2d subunit, as first-line treatments for chronic neuropathic pain. Throughout, chapters are accompanied with illustrative Tables and Figure providing a useful and comprehensive summary of the current state-of-play in this area of significant therapeutic interest. Work described here also provides a solid basis for future research in this important area.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Medicine.
Topical term or geographic name as entry element Cytology.
Topical term or geographic name as entry element Cell membranes.
Topical term or geographic name as entry element Neurobiology.
Topical term or geographic name as entry element Biomedicine.
Topical term or geographic name as entry element Biomedicine general.
Topical term or geographic name as entry element Neurobiology.
Topical term or geographic name as entry element Membrane Biology.
Topical term or geographic name as entry element Cell Physiology.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Mochida, Sumiko.
Relator term editor.
710 2# - ADDED ENTRY--CORPORATE NAME
Corporate name or jurisdiction name as entry element SpringerLink (Online service)
773 0# - HOST ITEM ENTRY
Title Springer eBooks
776 08 - ADDITIONAL PHYSICAL FORM ENTRY
Display text Printed edition:
International Standard Book Number 9789400763333
856 40 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier http://dx.doi.org/10.1007/978-94-007-6334-0
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme
Item type E-Book
Copies
Price effective from Permanent location Date last seen Not for loan Date acquired Source of classification or shelving scheme Koha item type Damaged status Lost status Withdrawn status Current location Full call number
2014-04-08AUM Main Library2014-04-08 2014-04-08 E-Book   AUM Main Library610
Languages: 
English |
العربية