Neuron–Glia Interactions at the Neuromuscular Synapse

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Keith J. Todd and
  2. Richard Robitaille

Published Online: 7 OCT 2008

DOI: 10.1002/9780470032244.ch17

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

How to Cite

Todd, K. J. and Robitaille, R. (2006) Neuron–Glia Interactions at the Neuromuscular Synapse, in Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470032244.ch17

Author Information

  1. Département de Physiologie, Université de Montréal, Centre de Recherche en Sciences Neurologiques, P O Box 6128 Station Centre-Ville, Montréal, Québec, H3C 3J7, Canada

  1. This paper was presented at the symposium by Richard Robitaille, to whom correspondence should be addressed.

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 21 APR 2006

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470018606

Online ISBN: 9780470032244

SEARCH

Keywords:

  • neuromuscular junction (NMJ) and acetylcholine (ACh);
  • neuromuscular synapse;
  • purinergic PSC signalling;
  • PSC Ca2+ responses and muscarinic ACh receptors (mAChRs);
  • purines and synapse–glia interactions

Summary

The contribution of glial cells in the regulation of the transfer of information in CNS and PNS is now increasingly recognized. Perisynaptic Schwann cells (PSCs), glial cells at the neuromuscular junction (NMJ), have proven to be an exceptionally important model for studying these roles. PSCs surround nerve terminals at the NMJ and are activated by transmitter release in a frequency-dependent manner. All of these receptors, except one type, are coupled to G proteins and can be regrouped into two categories: activators and modulators of PSCs. In the former category are muscarinic (unknown subtype) and purinergic receptors (P2X and P2Y). In the latter category are adenosine (A1), Substance P (NK-1) and CGRP receptors. All receptors coupled to G proteins induce the release of Ca2+from internal stores. In return for this activation, PSCs modulate synaptic activity and short-term plasticity. In this review, we will focus on the role of purines in the induction of glial cell activity and their possible involvement in the modulation of synaptic transmission as a result of the synaptic-induced glial activity.