Estrogen-induced signaling mechanisms involed in the establishment of the sexual dimorphysm of the rat brain

在大鼠脑内，视前内侧区（POA）的性二形核（SDN）是控制性二形行为和生理功能的主要部位。在胚胎第18天左右开始的关键期内，暴露于17 β-雌二醇（E2）可形成二态性。为了探讨E2诱导性别差异的关键因素和机制，我们从出生时接受E2处理的雌性大鼠脑片中提取了含有SDN的总RNA，并将其用于DNA微阵列。蛋白激酶C-δ（PKC-δ）基因的表达被E2显著上调。然后，我们通过Western印迹和免疫组织化学检查了PKC-δ的下游效应物，发现PKC-δ/Rac 1/LIMK 1/cofilin通路参与其中。这项工作表明，肌动蛋白动力学增强的细胞迁移是一个线索，创造性的二型性在POA的大鼠脑。

In the rat brain, the sexually dimorphic nucleus (SDN) of the medial preoptic area (POA) is a major site for controlling sexual dimorphic behavior and physiological functions. The dimorphism is formed by the exposure to 17beta;-estradiol (E2) during the critical period, which begins around embryonic day 18. In order to explore key factors and mechanisms involved in the establishment of sex differences in response to E2, we prepared total RNA from brain slices containing SDN from female rats treated with E2 at birth, which was subjected to DNA microarray. The expression of the gene for protein kinase C-delta; (PKC-delta;) was significantly up-regulated by E2. We then examined the downstream effectors of PKC-delta; by Western blotting and immunohistochemistry, and found the involvement of the PKC-delta;/Rac1/LIMK1/cofilin pathway. This work demonstrated that cell migration enhanced by actin dynamics is a cue to create the sexual dimorphism in POA of the rat brain.