Acetylcholine reduces the slow calcium current in embryonic skeletal muscle cells in culture

Abstract

Xenopus skeletal muscle cells when grown in culture develop a slow inward calcium current that is sensitive to dihydropyridines. Acetylcholine (ACh, 10 microM) applied through a puffer pipette caused a large inward current in these cells (at the holding potential) through the nicotinic receptor channels and reduced the inward calcium current (during a step depolarization to 0 mV). After the ACh application was discontinued the holding current rapidly returned to pre-ACh levels (20 s) whereas the calcium current showed a slow, partial recovery to pre-ACh levels. Outward potassium current was also reduced during the application of ACh but recovered completely after ACh was discontinued. The effect of ACh on the calcium current was not mimicked by muscarine (100 microM) and was absent when 10 micrograms/ml alpha-bungarotoxin was added to the bath suggesting that the decrease in calcium current was mediated by current through the nicotinic receptor.

Activation of nicotinic acetylcholine receptors increases the rate of fusion of cultured human myoblasts.

“…In addition to the well-known effect on the cationic channel, activation of nAChR can induce metabotropic effects. For example, ACh applied on cultured Xenopus skeletal muscle reduced an inward calcium current as well as an outward potassium current, presumably through a metabotropic effect of the nAChR (Moody-Corbett & Virgo, 1993). Furthermore, ACh applied on cultured mouse myotubes in the absence of extracellular calcium raised intracellular calcium concentration, and this calcium mobilization was concomitant with inositol 1,4,5-trisphosphate accumulation (Giovanelli, Grassi, Mattei, Mileo & Eusebi, 1991; In an attempt to distinguish between metabotropic and ionotropic effects of nAChR activation on myoblast fusion, decamethonium was tested.…”