Androgen regulation of the nicotinic acetylcholine receptor-ionic channel in a hormone-dependent skeletal muscle.
The trophic influence of testosterone on the nicotinic acetylcholine receptor-ionic channel (AChR) was studied in the levator ani (LA) muscle of adult male rats (120 days) intact (C) or gonadectomized when 90 days old (G). In the indirectly elicited muscle twitch, the LA from G rats was less sensitive to d-tubocurarine (0.1-1 microM) than control muscles (IC25: C = 0.30 microM, G = 0.46 microM). In G rats, the amplitude of neurally evoked endplate currents (EPC) was reduced by 70%, but the EPC time constant was not changed. Maximal junctional binding of [125I]alpha-bungarotoxin in the LA (C: 72.5 +/- 13.2 amol/endplate) was reduced by 1.8-fold in LA from G rats, with no change of the association rate constant (C: 5.64 +/- 1.29 10(6) M-1 min-1). The results indicate that testosterone deprivation reduces the junctional AChR density in the rat LA without modifying the binding properties of the receptor.
Souccar
C
C
Departamento de Farmacologia, Escola Paulista de Medicina, São Paulo, Brasil.
Yamamoto
L A
LA
Gonçalo
M C
MC
Lapa
A J
AJ
D000818:Animals; D001665:Binding Sites; D008297:Male; D008564:Membrane Potentials; D009045:Motor Endplate / Q000502:physiology*; D009132:Muscles / Q000502:physiology*; D009919:Orchiectomy; D051381:Rats; D011978:Receptors, Nicotinic / Q000187:drug effects*; D013739:Testosterone / Q000494:pharmacology*; D014403:Tubocurarine / Q000494:pharmacology
D011978:Receptors, Nicotinic; D013739:Testosterone; D014403:Tubocurarine