Thesis (Ph.D.) - Indiana University, Neuroscience, 2014Early hormone exposure is required for the development of many neural structures across a variety of species. The spinal nucleus of the bulbocavernosus (SNB), a motor nucleus that controls erections and ejaculations in male rats, requires gonadal hormones for typical development. While the masculinization of many features of the SNB neuromuscular system is androgen-dependent, dendrogenesis requires estrogens during a developmentally restricted critical period. This estrogen-dependent SNB dendrite growth is mediated by estrogen receptors (ERs) in the SNB target musculature (the bulbocavernosus, BC). I have demonstrated that ERα expression in BC extra-muscle fiber cells defines the critical period for estrogen-dependent SNB dendrite growth, and estradiol treatment during ERα expression in these extra-muscle fiber cells fully masculinizes SNB dendrites. Further, BC ERα expression is sensitive to gonadal hormones: Castration dramatically upregulates the density of extra-muscle fiber cell ERα. Brief estradiol treatment during heightened ERα expression results in rapid, robust dendritic growth, suggesting that the estrogen sensitivity of SNB dendrites is determined by ERα levels in the target musculature. I have shown that the castration-induced increase of ERα in the BC extends the critical period for estrogen-dependent SNB dendrogenesis, the first demonstration that SNB dendrites respond to estrogens outside the early postnatal period. I have shown that brain-derived neurotrophic factor (BDNF) is upregulated in the SNB target muscle following early postnatal castration, but immunolabeling for BDNF in SNB somata does not change. In both cases, estradiol treatment does not affect BDNF levels, demonstrating that while there may be a role for BDNF in early dendrite growth, estrogen-dependent dendrogenesis is not mediated by BDNF. Finally, I have shown that the ERα-expressing extra-muscle fiber cells in the BC are not satellite cells, and the specific cell type mediating early estrogen-dependent dendritic growth remains unknown. Together, these results elucidate the mechanisms of estrogen-dependent dendrite development in the SNB of male rats, establish the basis for the estrogen-sensitive critical period, and demonstrate the plasticity of estrogen-mediated dendrogenesis in the SNB.