Regulation of the number of α‐bungarotoxin binding sites in cultured chick myotubes by a 1,4 dihydropyridine calcium channel antagonist

Abstract

Calcium has been suggested as the second messenger link between skeletal muscle activity and AChR gene expression and synthesis. We have compared the concentrations of the Ca2+ channel antagonists D600 and nisoldipine needed both to block Ca2+ uptake into cultured myotubes and to increase AChR expression. The good correspondence between these two measurements and the use of the highly specific Ca2+ channel antagonist nisoldipine strengthens the hypothesis that AChR expression is regulated by levels of intracellular Ca2+.

Different mechanisms of Ca2+‐handling following nicotinic acetylcholine receptor stimulation, P2U‐purinoceptor stimulation and K+‐induced depolarization in C2C12 myotubes

“…A short-term increase in & Hodges-Savola, 1992). cellular Ca2`enhances the rate of desensitization of nicotine Stimulation of myotubes with the transmitter of motor acetylcholine receptors (nAChRs; Miledi, 1980), while a longneurones (acetylcholine), its co-transmitter ATP (Silinsky, term increase in Ca2" is involved in down-regulation of 1975) and depolarization of the myotubes have all been renAChRs (Smilowitz et al, 1988;Klarsfeld et al, 1989; ported to increase intracellular Ca2" in myotubes. In myotubes of different origin, the ACh-sensitive receptor which is involved in augmenting Ca2" has invariably been characterized ____________________ as the muscle type nicotinic receptor (Giovannelli et al, 1991; ceptors (P2-purinoceptors) is still largely based on their sensitivity to ATP analogues (Cusack & Hourani, 1990), because of the lack of a specific antagonist at cloned receptors (Webb et al, 1993;Lustig et al, 1993).…”