Efflux of acetylcholine in dimorphic skeletal muscle from castrated male rats

The effect of testosterone on motor neurons of dimorphic muscles is demostrable by increased frequency of miniature end-plate potentials (mepp) and decreased end-plate acetylcholinesterase activity observed in castrated rats. No change occurs in induced acetylcholine (ACh release. Although these muscles atrophy after castration there is no loss of muscle fibers. In the present study we reinvestigate the neuromuscular transmission in levator ani (LA) muscles from normal (N) adult (120 days) male rats and from rats castrated (C) 30 days before. The measurement of radioactive [3H]-choline was used to evaluate ACh release since it permits simultaneous estimation of quantal and non-quantal and non-quantal ACh release. The LA muscle was incubated with [3H]-choline (1µCi/ml) for 30 min and ACh efflux was measured after washout. The basal release of [3H]-choline (dpm total tissue radioactivity-1 number of fibers-1) was 296 ñ 33 and 156 ñ 24 in N and C, respectively. Induced ACh release (25 Hz, 5 min) was the same in N and C (653.19 ñ 66.46) and 496.62 ñ 68.67, respectively). These results indicate that castration increased nepp frequency buth reduced the total spontaneous release of ACh

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 malr 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 (0.1-1µM) than control muscles (IC25:C = 0.30µM,G=0.46µM). 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] alfa-bungarotoxin in the LA(C: 72.5 ñ 13.2 amol/endplate) was reduced by 18.8-fold in LA from G rats, with no change of the association rate constant (C: 5.64 ñ 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