Whole-Cell currents activated by bath applications of acetylcholine (ACh) (0-30 ?M) were recorded from patch-clamped myotubes of the mouse C2 cell line. Increasing concentrations of forskolin caused a dose-dependent fast decay of ACh-activated currents as compared to the long-lasting ACh-currents in control cells. The forskolin-induced modulation of nicotinic ACh receptor (nAChR) desensitization was proportional to the drug-induced elevation in the cyclic AMP (cAMP) cellular. Furthermore, an increase in the rate of decay of the ACh-current response, which paralleled an elevation in cAMP cellular content, was caused by treatment with a calcitonin gene-related peptide (1 ?M), 8-Br-cAMP) (0.5 mM), or by loading the myotubes with cAMP. These results therefore indicate that the desensitization of nAChR is a cAMP-related process in C2-myotubes. © 1990.
Regulation of acetylcholine receptor desensitization in mouse myotubes by cytosolic cyclic AMP
1990
Abstract
Whole-Cell currents activated by bath applications of acetylcholine (ACh) (0-30 ?M) were recorded from patch-clamped myotubes of the mouse C2 cell line. Increasing concentrations of forskolin caused a dose-dependent fast decay of ACh-activated currents as compared to the long-lasting ACh-currents in control cells. The forskolin-induced modulation of nicotinic ACh receptor (nAChR) desensitization was proportional to the drug-induced elevation in the cyclic AMP (cAMP) cellular. Furthermore, an increase in the rate of decay of the ACh-current response, which paralleled an elevation in cAMP cellular content, was caused by treatment with a calcitonin gene-related peptide (1 ?M), 8-Br-cAMP) (0.5 mM), or by loading the myotubes with cAMP. These results therefore indicate that the desensitization of nAChR is a cAMP-related process in C2-myotubes. © 1990.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
