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This Article Full Text Full Text (PDF) All Versions of this Article: 568/1/171    most recent jphysiol.2005.091439v1 Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Bandi, E. Articles by Lorenzon, P. Search for Related Content PubMed PubMed Citation Articles by Bandi, E. Articles by Lorenzon, P.

¹ Department of Physiology and Pathology and Centre for Neuroscience B.R.A.I.N., University of Trieste, Via A. Fleming 22, I-34127 Trieste, Italy
² Neurobiology Sector, International School for Advanced Studies (S.I.S.S.A), Via Beirut 2-4, I-34014 Trieste, Italy
³ Department of Cell Biology and Development, University ‘La Sapienza’, Piazzale A. Moro 5, I-00185 Rome, Italy

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.

(Received 14 June 2005; accepted after revision 14 July 2005; first published online 21 July 2005)
Corresponding author P. Lorenzon: Department of Physiology and Pathology, University of Trieste, Via A. Fleming 22, I-34127 Trieste, Italy. Email: pielle{at}dfpmail.units.it

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