Estrogen Induced Neuroplasticity in the Lordosis Pathway

描述（申请人摘要）： 下丘脑（VMH）是控制性行为的性二态性区域 以脊柱前凸反射为代表。雌性在性方面很容易接受 只有当雌激素存在时，腹外侧的雌激素受体 VMH的亚类（vlVMH）介导雌激素对性功能的影响。 行为相比之下，雄性大鼠不表现出脊柱前凸反应，甚至 被阉割后用雌激素治疗本提案的总体目标是 研究vlVMH中与雌激素作用相关的局部回路 与执行脊柱前凸反射的路径相连。具体目标是：1） 为了检验脊柱前凸相关传出神经分离的假设， 来自含雌激素受体的神经元，并受其支配; 2） 测试雌激素诱导脊柱前凸相关的树突棘的假设， vlVMH内有传出神经元，但无含雌激素受体的神经元; （3）检验性别差异在特定成分中的假设， VMH局部回路介导雌激素对脊柱的性别依赖性作用 VMH中的密度。这些方法将包括定量和定位 通过跨神经元追踪、常规顺行和 逆行追踪，共聚焦显微镜分析树突棘密度 充满荧光黄的细胞，以及这些技术与 免疫细胞化学这些研究的结果可能会阐明 雌激素对神经功能的影响

DESCRIPTION (applicant's abstract): The ventromedial nucleus of the hypothalamus (VMH) is a sexually dimorphic region that controls sexual behavior in female rats, typified by the lordosis reflex. Females are sexually receptive only when estrogen is present, and estrogen receptors in the ventrolateral subdivision of the VMH (vlVMH) mediate the effects of estrogen on sexual behavior. Male rats, in contrast, do not exhibit the lordosis response, even when castrated and treated with estrogen. The general goal of this proposal is to investigate the local circuitry in the vlVMH that couples estrogen action with the pathways that execute the lordosis reflex. The specific aims are: 1) To test the hypothesis that the lordosis-relevant efferents are segregated from, and are innervated by, the estrogen receptor-containing neurons; 2) To test the hypothesis that estrogen induces dendritic spines in lordosis-relevant efferent neurons, but not estrogen receptor-containing neurons, in the vlVMH; and 3) To test the hypothesis that sex differences in specific components of the VMH local circuitry mediate the sex-dependent effect of estrogen on spine density in the VMH. The methods will include quantification and localization of neurons visualized by transneuronal tracing, conventional anterograde and retrograde tracing, confocal microscopic analysis of dendritic spine density on Lucifer yellow-filled cells, and the combination of these techniques with immunocytochemistry. The results of these studies may illuminate the effects of estrogen on neural function.