The spinal cord of rats contains the sexually dimorphic motoneurons of the spinal nucleus of the bulbocavernosus (SNB). In males, SNB dendrites fail to grow after castration, but androgen or estrogen treatment supports dendritic growth in castrated males. Estrogenic support of SNB dendrite growth is mediated by estrogen receptors (ER) in the target muscle. ER expression in cells lacking a basal lamina (referred to as extra-muscle fiber cells) of the SNB target musculature coincides with the period of estrogen-dependent SNB dendrite growth. In the SNB target muscle, extra-muscle fiber ER expression declines with age and is typically absent after postnatal (P) day 21 (P21). Given that estradiol downregulates ER in skeletal muscle, we tested the hypothesis that depleting gonadal hormones would prevent the postnatal decline in ER expression in the SNB target musculature. We castrated male rats at P7 and assessed ER immunolabeling at P21; ER expression was significantly greater in castrated males compared with normal animals. Because ER expression in SNB target muscles mediates estrogen-dependent SNB dendrogenesis, we further hypothesized that the castration-induced increase in muscle ER would heighten the estrogen sensitivity of SNB dendrites. Male rats were castrated at P7 and treated with estradiol from P21 to P28; estradiol treatment in castrates resulted in dendritic hypertrophy in SNB motoneurons compared with normal males. We conclude that early castration results in an increase in ER expression in the SNB target muscle, and this upregulation of ER supports estrogen sensitivity of SNB dendrites, allowing for hypermasculinization of SNB dendritic arbors. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 73: 921-935, 2013
