Androgen mitigates axotomy-induced decreases in calbindin expression in motor neurons.

摘要: Androgens can rescue axotomized motor neurons from cell death. Here we examine a possible mechanism for this trophic action in juvenile Xenopus laevis: regulation of calciumbinding protein, calbindin, after axotomy. Western analysis revealed that monoclonal antibody to calbindin D specifically recognizes single ;28 kDa band X. laevis CNS and rat cerebellum. Retrograde transport peroxidase combined with immunohistochemistry demonstrated somata, axons, synaptic terminals laryngeal nucleus (N.) IX‐X are calbindin-positive. The number calbindin-positive cells was compared the intact sides N.IX‐X gonadectomized males were either hormonally untreated or DHT-treated 1 month. Although axotomy decreased by 86% males, decrease only 56% animals. Compared animals, calbindin-labeled increased both (14%) (75%). We conclude decreases DHT enhances immunoreactivity N.IX‐X. Axotomy-induced precedes loss may impair capacity regulate cytoplasmic calcium. Androgen-mediated maintenance expression is thus candidate cellular hormone target neurons.