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Autocrine activation of nicotinic acetylcholine receptors contributes to Ca 2+ spikes in mouse myotubes during myogenesis

Autocrine activation of nicotinic acetylcholine receptors contributes to Ca 2+ spikes in mouse... It is widely accepted that nicotinic acetylcholine receptor (nAChR) channel activity controls myoblast fusion into myotubes during myogenesis. In this study we explored the possible role of nAChR channels after cell fusion in a murine cell model. Using videoimaging techniques we showed that embryonic muscle nAChR channel openings contribute to the spontaneous transients of intracellular concentration of Ca2+ ((Ca2+)i) and to twitches characteristic of developing myotubes before innervation. Moreover, we observed a choline acetyltransferase immunoreactivity in the myotubes and we detected an acetylcholine‐like compound in the extracellular solution. Therefore, we suggest that the autocrine activation of nAChR channels gives rise to (Ca2+)i spikes and contractions. Spontaneous openings of the nAChR channels may be an alternative, although less efficient, mechanism. We report also that blocking the nAChRs causes a significant reduction in cell survival, detectable as a decreased number of myotubes in culture. This led us to hypothesize a possible functional role for the autocrine activation of the nAChRs. By triggering mechanical activity, such activation could represent a strategy to ensure the trophism of myotubes in the absence of nerves. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Autocrine activation of nicotinic acetylcholine receptors contributes to Ca 2+ spikes in mouse myotubes during myogenesis

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References (36)

Publisher
Wiley
Copyright
© 2005 The Journal of Physiology © 2005 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/jphysiol.2005.091439
pmid
16037088
Publisher site
See Article on Publisher Site

Abstract

It is widely accepted that nicotinic acetylcholine receptor (nAChR) channel activity controls myoblast fusion into myotubes during myogenesis. In this study we explored the possible role of nAChR channels after cell fusion in a murine cell model. Using videoimaging techniques we showed that embryonic muscle nAChR channel openings contribute to the spontaneous transients of intracellular concentration of Ca2+ ((Ca2+)i) and to twitches characteristic of developing myotubes before innervation. Moreover, we observed a choline acetyltransferase immunoreactivity in the myotubes and we detected an acetylcholine‐like compound in the extracellular solution. Therefore, we suggest that the autocrine activation of nAChR channels gives rise to (Ca2+)i spikes and contractions. Spontaneous openings of the nAChR channels may be an alternative, although less efficient, mechanism. We report also that blocking the nAChRs causes a significant reduction in cell survival, detectable as a decreased number of myotubes in culture. This led us to hypothesize a possible functional role for the autocrine activation of the nAChRs. By triggering mechanical activity, such activation could represent a strategy to ensure the trophism of myotubes in the absence of nerves.

Journal

The Journal of Physiology – Wiley

Published: Oct 1, 2005

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