Brain mechanism mediating fasting-induced suppression of reproductive function

介导禁食引起的生殖功能抑制的脑机制

• 批准号: 08660342
• 负责人: TSUKAMURA Hiroko
• 金额: $ 1.54万
• 依托单位: Nagoya University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08660342/
• 关键词: luteinizing hormone; fasting stress; estrogen; estrogen receptor; A2 region of solitary tract nucleus; paraventricular nucleus; noradrenergic neurons; 延髄孤束核A2領域; ノルアドレナリン作働性神経

Fasting-stress profoundly suppresses luteinizing hormone (LH) secretion in the rat in a estrogen dependent manner. It has been demonstrated that this suppression is mediated by noradrenergic neurons projecting to the hypothalamic paraventricular nucleus (PVN). The present research aimed to investigate further brain mechanism mediating the fasting-induced suppression of LH release.Forty-eight h fasting significantly increased numbers of estrogen receptor-containing cells in both the PVN and A2 region of solitary tract nucleus (NTS) in the lower brain stem. Acute infusion of estrogen into the PVN caused an inhibition of pulsatile LH release only in the 48-h fasted ovariectomized (OVX) rats, but not in the ad lib-fed OVX rats. On the other hand, the estrogen infusion into the NTS did not affect LH secretion. The estrogen infusion into the both nuclei did not affect the noradrenaline release in the PVN.These results suggest that fasting induces estrogen receptor expression in the PVN where estrogen acts to suppresses LH secretion without affecting noradrenaline release.It has demonstrated that intravenous injection of 2-deoxyglucose (2DG), a glucose antagonist, suppressed pulsatile LH release in OVX rats in a dose-dependent manner and that estrogen enhanced the inhibitory effect of 2DG on LH pulses. Furthermore, 2DG induced noradrenaline release in the PVN,and local injection of catecholamine synthesis inhibitor into the PVN blocked 2DG-induced suppression of LH secretion. These results suggest that suppression of LH release by lowered glucose availability is mediated y noradrenergic neurons projecting the PVN.

禁食应激以雌激素依赖性方式深刻抑制大鼠黄体生成素（LH）的分泌。已经证明，这种抑制是由投射到下丘脑室旁核（PVN）的去甲肾上腺素能神经元介导的。本研究旨在进一步研究介导禁食引起的 LH 释放抑制的脑机制。禁食 48 小时，下丘脑孤束核 (NTS) 的 PVN 和 A2 区含有雌激素受体的细胞数量显着增加。脑干。雌激素急性输注到PVN中仅在48小时禁食卵巢切除(OVX)大鼠中引起脉动LH释放的抑制，但在自由喂养的OVX大鼠中则没有。另一方面，将雌激素输注到NTS中并不影响LH的分泌。雌激素输注到两个核中并不影响PVN中去甲肾上腺素的释放。这些结果表明，禁食诱导PVN中雌激素受体的表达，其中雌激素起到抑制LH分泌的作用，而不影响去甲肾上腺素的释放。已经证明，静脉注射2-脱氧葡萄糖 (2DG) 是一种葡萄糖拮抗剂，以剂量依赖性方式抑制 OVX 大鼠的脉动性 LH 释放，并且雌激素增强了2DG 对 LH 脉冲的抑制作用。此外，2DG诱导PVN中去甲肾上腺素释放，并且向PVN局部注射儿茶酚胺合成抑制剂阻断2DG诱导的LH分泌抑制。这些结果表明，通过降低葡萄糖利用率来抑制 LH 释放是由投射 PVN 的去甲肾上腺素能神经元介导的。