Regulation of acetylcholine receptor desensitization in mouse myotubes by cytosolic cyclic AMP.
Whole-cell currents activated by bath applications of acetylcholine (ACh) (10-30 microM) 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 content. 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 microM), 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.
Giovannelli
A
A
Dipartimento di Medicina Sperimentale Università dell'Aquila, Italy.
Farini
D
D
Gauzzi
M C
MC
Alema
S
S
Eusebi
F
F
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D002460:Cell Line; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism* / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004594:Electrophysiology; D051379:Mice; D009132:Muscles / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D011950:Receptors, Cholinergic / Q000378:metabolism*
D011950:Receptors, Cholinergic; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D000242:Cyclic AMP; D015740:Calcitonin Gene-Related Peptide