Abstract
In mouse C2C12 myotubes acetylcholine (ACh) elevates the concentration of myoplasmic Ca2+ ([Ca2+]i) by inducing Ca2+ influx through transmittergated and voltage-gated channels, and by mobilizing Ca2+ from internal stores. The relative contribution of each of these ACh-activated sources to the global [Ca2+]i elevation was estimated. We found that Ca2+ entry through voltage- and ACh-gated channels accounts for roughly 80% of the total [Ca2+]i increment, while mobilization from internal caffeine-sensitive and inositol-trisphosphate (Ins P3-) sensitive stores contributes the remaining 20% to the maximal [Ca2+]i increment. Furthermore, we found that ACh-induced mobilization from Ins P3-sensitive stores also develops in embryonic chick myotubes. The differential importance of the Ca2+ signalling pathways activated by ACh during myogenesis is discussed.
Original language | English |
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Pages (from-to) | 340-345 |
Number of pages | 6 |
Journal | Pflugers Archiv European Journal of Physiology |
Volume | 428 |
Issue number | 3-4 |
DOIs | |
Publication status | Published - Oct 1994 |
Keywords
- Acetylcholine
- Acetylcholine nicotinic receptor
- C2C12 myotube
- Calcium
- Metabotropic function
ASJC Scopus subject areas
- Physiology