Testosterone increases acetylcholine receptor number in the “levator ani” muscle of the rat

Abstract

The "levator ani" muscle of male rats provides a neuromuscular system in which both the muscle and its motoneurons have high levels of androgen receptors. Two weeks of castration caused a 48% loss of acetylcholine receptors in this muscle. One week of testosterone propionate injections initiated on week after castration increased receptor number by 27% over untreated castrate levels. These changes paralleled changes in muscle protein content. In contrast, castration and testosterone treatments of castrates had no effect on total. Triton X-100-extractable acetylcholinesterase activity. This system may provide a useful model of synaptic plasticity.

Lactate dyscrasia: a novel explanation for amyotrophic lateral sclerosis

“…Finally, in Xenopus laevis, females have stronger laryngeal synapses than males, and synapse strength is estrogen dependent and the laryngeal neuromuscular synapse is the final effector for sexually differentiated song production. Immunocytochemistry and Western blots confirmed the presence of estrogen receptor protein in laryngeal muscle fibers (Bleisch et al, 1982). Together, these observations suggest a prominent role for sex steroids in the normal functioning of neurons and muscles in the NMJ.…”

“…In addition, there is strong evidence for the fact that testosterone via its receptor may regulate the coupling mechanisms between Ca v2.2 channels and neurotransmitter release at the neuromuscular junctions of bulbocavernosus and levator ani muscles motoneurons (Nudler et al, 2005). Earlier results have shown that testosterone deprivation reduces the junctional acetylcholine receptor density and androgens modulate endplate size and acetylcholine ACh receptor density at synapses in rat levator ani muscle (Bleisch and Harrelson, 1989;Bleisch et al, 1982;Souccar et al, 1991). Finally, in Xenopus laevis, females have stronger laryngeal synapses than males, and synapse strength is estrogen dependent and the laryngeal neuromuscular synapse is the final effector for sexually differentiated song production.…”

The spinal nucleus of the bulbocavernosus: Firsts in androgen-dependent neural sex differences

“…These anabolic effects of androgens involve changes in perineal muscle fiber size, without a change in fiber number (Venable, 1966). Androgens in adulthood also maintain BC/LA neuromuscular junction size (Bleisch and Harrelson, 1989;Balice-Gordon et al, 1990;Lubischer and Bebinger, 1999), acetylcholine receptor number (Bleisch et al, 1982;Bleisch and Harrelson, 1989), and peripheral nerve activity (Fargo et al, 2003).…”

Androgenic, but not estrogenic, protection of motoneurons from somal and dendritic atrophy induced by the death of neighboring motoneurons

“…For example, levels of immunoreactivity for the ciliary neurotrophic factor receptor α (Forger et al, 1998) and BCL-2 (Zup and Forger, 2002) are androgendependent in SNB motoneurons, as are levels of mRNA expression for the major cytoskeletal elements β-actin (Matsumoto et al, 1992) and β-tubulin (Matsumoto et al, 1993). Moreover, the SNB target muscles also contain high numbers of androgen receptors (Monks et al, 2004), and androgens regulate a variety of characteristics of these muscles, including fiber size (Venable, 1966), neuromuscular junction size (Bleisch and Harrelson, 1989;Balice-Gordon et al, 1990), acetylcholine receptor number (Bleisch et al, 1982;Bleisch and Harrelson, 1989), muscle excitability (Foster and Sengelaub, 2004), and the number of functional calcium channels at the neuromuscular junction (Nudler et al, 2005). These results raise the possibility that the neuroprotective effects of androgens after saporin-induced motoneuron depletion in this system could be mediated by the muscle (Fargo and Sengelaub, 2004a,b).…”