QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Georgiou, J. Articles by Charlton, M. P. Search for Related Content PubMed PubMed Citation Articles by Georgiou, J. Articles by Charlton, M. P.

 Previous Article  |  Next Article 

The Journal of Neuroscience, May 15, 1999, 19(10):3836-3846

Muscarinic Control of Cytoskeleton in Perisynaptic Glia

John Georgiou¹, Richard Robitaille², and Milton P. Charlton¹

¹ Department of Physiology, Medical Research Council Group in Nerve Cells and Synapses, and Neuroscience Network, University of Toronto, Toronto, Ontario, Canada M5S 1A8, and ² Centre de Recherche en Sciences Neurologiques, and Département de Physiologie, Université de Montréal, Montréal, Québec, Canada H3C 3J7

Similar to astrocytes at CNS synapses, perisynaptic Schwann cells (PSCs) surround nerve terminals at the neuromuscular junction (NMJ). These special teloglial cells are sensitive to neurotransmitters and upregulate glial fibrillary acidic protein (GFAP) when deprived of synaptic activity. We found that activation of muscarinic acetylcholine receptors (mAChRs) at PSCs, but not purinergic (ATP and adenosine) or peptidergic [substance P (SP) and calcitonin gene-related peptide (CGRP)] receptors, prevented this upregulation. When applied onto single PSCs, muscarine evoked Ca²⁺ responses that fatigued but prevented upregulation of this glial cytoskeletal protein. Application of ATP onto single PSCs evoked Ca²⁺ signals that showed little fatigue, and GFAP upregulation occurred. Thus, Ca²⁺ signals alone cannot prevent GFAP upregulation in the PSCs. After blockade of cholinergic receptors by gallamine, neuronal activity was not effective in maintaining low GFAP levels in the perisynaptic glia. Last, immunohistochemistry disclosed mAChRs on PSCs and nearby fibroblasts. Thus, acetylcholine secreted by the nerve terminal acts on the PSCs via mAChRs to regulate GFAP. Cytoskeletal changes may influence perisynaptic glial functions, including growth, remodeling, and modulation of the synapse.

Key words: nerve-glia signaling; nerve terminal; glial cell; transmitter; synapse; neuromuscular junction; terminal Schwann cell; GFAP; muscarine; muscarinic acetylcholine receptors; Ca²⁺; cytoskeleton; plasticity

---

Copyright © 1999 Society for Neuroscience  0270-6474/99/19103836-11$05.00/0

This article has been cited by other articles:

				Z. Feng, S. Koirala, and C.-P. Ko Synapse-Glia Interactions at the Vertebrate Neuromuscular Junction Neuroscientist, October 1, 2005; 11(5): 503 - 513. [Abstract] [PDF]

				D. S. Auld and R. Robitaille Perisynaptic Schwann Cells at the Neuromuscular Junction: Nerve- and Activity-Dependent Contributions to Synaptic Efficacy, Plasticity, and Reinnervation Neuroscientist, April 1, 2003; 9(2): 144 - 157. [Abstract] [PDF]

				D. Rochon, I. Rousse, and R. Robitaille Synapse-Glia Interactions at the Mammalian Neuromuscular Junction J. Neurosci., June 1, 2001; 21(11): 3819 - 3829. [Abstract] [Full Text] [PDF]

				S. L. Tam, V. Archibald, B. Jassar, N. Tyreman, and T. Gordon Increased Neuromuscular Activity Reduces Sprouting in Partially Denervated Muscles J. Neurosci., January 15, 2001; 21(2): 654 - 667. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help