Activation of the nicotinic acetylcholine receptor mobilizes calcium from caffeine-insensitive stores in C2C12 mouse myotubes
✍ Scribed by F. Grassi; A. Giovannelli; S. Fucile; F. Eusebi
- Publisher
- Springer
- Year
- 1993
- Tongue
- English
- Weight
- 974 KB
- Volume
- 422
- Category
- Article
- ISSN
- 0031-6768
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✦ Synopsis
In cultured mouse C2C12 myotubes, digital Ca 2+ imaging fluorescence microscopy using the acetoxymethyl ester of Fura-2, Fura-2-AM, showed that, in the absence of extracellular Ca 2+, acetylcholine (ACh) and nicotine, but not muscarine, raised the intracellular concentration of Ca 2 + ([Ca 2 +]i) by about tenfold. AChinduced Ca 2 + 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 Ca z+ from the ryanodine-sensitive stores of the sarcoplasmic reticulum, did not interfere with the ACh-induced [Ca 2 +]i increase. Ca 2+ 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 [Ca 2 +~i increase. Possible mechanisms linking the current flowing through the nAChR pore to [Ca 2 +]i increase are discussed.