Activation of the nicotinic acetylcholine receptor mobilizes calcium from caffeine-insensitive stores in C2C12 mouse myotubes

F. Grassi, A. Giovannelli, S. Fucile, F. Eusebi

Research output: Contribution to journalArticlepeer-review

Abstract

In cultured mouse C2C12 myotubes, digital Ca2+ imaging fluorescence microscopy using the acetoxymethyl ester of Fura-2, Fura-2-AM, showed that, in the absence of extracellular Ca2+, acetylcholine (ACh) and nicotine, but not muscarine, raised the intracellular concentration of Ca2+ ([Ca2+]i) by about tenfold. AChinduced Ca2+ mobilization was prevented by thapsigargin, a drug known to deplete inositol 1,4,5-trisphosphate (InsP3)-sensitive stores, and was concomitant with InsP3 accumulation. Caffeine, which releases Ca2+ from the ryanodine-sensitive stores of the sarcoplasmic reticulum, did not interfere with the ACh-induced [Ca2+]i increase. Ca2+ mobilization was also inhibited when myotubes were depolarized by high K+, or when extracellular Na+ was omitted. Nicotinic ACh receptor (nAChR) stimulation lowered intracellular pH with a time course slower than the [Ca2+]i increase. Possible mechanisms linking the current flowing through the nAChR pore to [Ca2+]i increase are discussed.

Original languageEnglish
Pages (from-to)591-598
Number of pages8
JournalPflugers Archiv European Journal of Physiology
Volume422
Issue number6
DOIs
Publication statusPublished - Mar 1993

Keywords

  • Acetylcholine
  • C2C12 myotubes
  • Calcium
  • Inositol 1,4,5-trisphosphate
  • Nicotine
  • Nicotinic acetylcholine receptor

ASJC Scopus subject areas

  • Physiology

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