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Modulation of Presynaptic Calcium Channels

  • Gary Stephens
  • Sumiko Mochida

Table of contents

  1. Front Matter
    Pages i-xii
  2. Overview

    1. Front Matter
      Pages 1-1
  3. Interaction Partners of Calcium Channels

    1. Front Matter
      Pages 27-27
    2. Gerald J. Obermair, Bernhard E. Flucher
      Pages 29-59
    3. Akito Nakao, Mitsuru Hirano, Yoshinori Takada, Shigeki Kiyonaka, Yasuo Mori
      Pages 79-99
    4. Pierre Charnet, Frédérique Scamps, Matthieu Rousset, Claudine Menard, Michel Bellis, Thierry Cens
      Pages 131-149
    5. Maxine Dibué, Etienne E. Tevoufouet, Felix Neumaier, Andreas Krieger, Alexandra Kiel, Dimitar Evdokimov et al.
      Pages 151-174
    6. Michel Bellis, Thierry Cens, Pierre Charnet, Matthieu Rousset
      Pages 175-198
  4. Mechanisms of Studying Calcium Channel Effects

    1. Front Matter
      Pages 199-199
    2. Holger Taschenberger, Kun-Han Lin, Shuwen Chang
      Pages 201-221
    3. Giovanna Bucci, Sumiko Mochida, Gary Stephens
      Pages 223-240
  5. Calcium Channel Therapeutics

  6. Back Matter
    Pages 363-365

About this book

Introduction

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.

Keywords

CNS disease calcium channels genetic disease presynaptic mechanisms synaptic transmission

Editors and affiliations

  • Gary Stephens
    • 1
  • Sumiko Mochida
    • 2
  1. 1., School of PharmacyUniversity of ReadingReadingUnited Kingdom
  2. 2., Department of PhysiologyTokyo Medical UniversityTokyoJapan

Bibliographic information