SUPPRESSION OF SODIUM-CHANNEL FUNCTION IN DIFFERENTIATING C2 MUSCLE-CELLS STABLY OVEREXPRESSING RAT ANDROGEN RECEPTORS

Citation
Js. Tabb et al., SUPPRESSION OF SODIUM-CHANNEL FUNCTION IN DIFFERENTIATING C2 MUSCLE-CELLS STABLY OVEREXPRESSING RAT ANDROGEN RECEPTORS, The Journal of neuroscience, 14(2), 1994, pp. 763-773
Citations number
79
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
14
Issue
2
Year of publication
1994
Pages
763 - 773
Database
ISI
SICI code
0270-6474(1994)14:2<763:SOSFID>2.0.ZU;2-M
Abstract
Differentiation of skeletal muscle and the formation of the neuromuscu lar junction are regulated by steroid hormones. The effects of androge ns on ion channel proteins central to neuromuscular signalling have be en investigated in differentiating mouse muscle C2 cells and in C2 cel ls that stably overexpress the rat androgen receptor (AR) cDNA. Neithe r the expression nor function of ACh receptors was regulated by androg enic actions in these cells. However, voltage-dependent sodium (Na) cu rrent density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpr ess the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influe nce posttranscriptional processing of Na channels in differentiating C 2 cells.