Brain mechanism by which estrogen enhances fasting-induced suppression of reproductive function

禁食应激以雌激素依赖的方式显著抑制大鼠黄体生成素（LH）的分泌。研究表明，禁食48小时显著增加下丘脑室旁核（PVN）和下脑干孤立束核（NTS） A2区雌激素受体细胞的数量。本研究旨在探讨雌激素增强空腹抑制黄体生成素分泌的脑机制。研究了去卵巢大鼠PVN和NTS中雌激素受体α (estrogen receptor α, ERα)细胞数量的变化。在NTS和PVN A2区酪氨酸羟化酶（TH）和多巴胺-β-羟化酶(DBH) -ir神经元中ERα免疫反应性的解剖关系也被确定。与未禁食的对照组相比，空腹30小时后PVN和NTS的ERα-ir细胞数量显著增加，并持续到48小时。葡萄糖活化也显著增加了这些细胞核中的ERα-ir细胞数量。48 h空腹和糖解作用显著增加含er α的TH-/DBH-ir细胞。在PVN中，大多数ERα-ir神经元与th和DBH-ir变异并置。这些结果表明，ERα在禁食开始后的特定时间在特定脑区表达，葡萄糖利用率降低可能是介导这种禁食诱导的ERα表达变化的关键信号。此外，A2区和PVN的去甲肾上腺素能神经元和ERα-ir神经元的解剖关系可能提示雌激素在增加A2区去甲肾上腺素能神经元的活性和PVN对来自下脑干的去甲肾上腺素能输入的敏感性，从而增强禁食时LH分泌的抑制作用。

Fasting-stress profoundly suppresses luteinizing hormone (LH) secretion in the rat in an estrogen dependent manner. It has been demonstrated that 48-h fasting significantly increased numbers of estrogen receptor-containing cells in both the hypothalamic paraventricular nucleus (PVN) and A2 region of solitary tract nucleus (NTS) in the lower brain stem. The present research aimed to investigate the brain mechanism by which estrogen enhances fasting-induced suppression of LH secretion.Changes in the number of estrogen receptor α (ERα) -containing cells by fasting and pharmacological glucoprivation were investigated in the PVN and NTS of ovariectomized rats. It has been also determined that the anatomical relationship of ERα immunoreactivity within tyrosine hydroxylase (TH) -and dopamine-β-hydroxylase (DBH) -ir neurons in the A2 region of the NTS and the PVN. The number of ERα-ir cells significantly increased after 30 h from the onset of fasting in the PVN and NTS compared with the unfasted controls and was sustained until 48 h. Glucoprivation also significantly increased the number of ERα-ir cells in these nuclei. Forty-eight h fasting and glucoprivation significantly increased ERα-containing TH-/DBH-ir cells. In the PVN, most ERα-ir neurons were juxtaposed with TH-and DBH-ir varicosities. These results suggest that ERα is expressed in specific brain regions at a defined time from the onset of fasting, and that lowered glucose utilization might be the key signal mediating this fasting-induced changes in ERα expression. In addition, the anatomical relationship of noradrenergic and ERα-ir neurons in the A2 region and PVN may suggest a role for estrogen in increasing the activity of noradrenergic neurons in the A2 region and the sensitivity of the PVN to noradrenergic input arising from the lower brainstem and thereby augmenting the suppression of LH secretion during fasting.