Hypothalamic mechanisms mediating glutamate effects on the hypothalamo-pituitary-adrenocortical axis
Hypothalamic mechanisms mediating glutamate effects on the hypothalamo-pituitary-adrenocortical axis
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DOI：
10.1007/bf01291881
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发表时间：
1997-01-01
影响因子：
3.3
通讯作者：
Weidenfeld, J
中科院分区：
文献类型：
--
作者：
Feldman, S;Weidenfeld, J
在雄性大鼠中研究了下丘脑室旁核（PVN）局部给予谷氨酸对下丘脑-垂体肾上腺皮质（HPA）轴的影响。谷氨酸导致正中隆起 (ME) 的 CRH-41 消耗，并随后导致 ACTH 和皮质酮 (CS) 血清水平升高。在用全身地塞米松（dex）预处理的大鼠中，这些作用被完全抑制。给予糖皮质激素受体拮抗剂RU-38486消除了dex对肾上腺皮质放电的抑制作用。此外，分别给予腹侧去甲肾上腺素能束或中缝核的特定神经毒素会消耗下丘脑去甲肾上腺素（NE）和血清素（5-HT），抑制PVN谷氨酸给药后血清ACTH和CS的反应。这些数据表明谷氨酸通过将 ME CRH-41 释放到门静脉循环中来刺激 HPA 轴。这种反应对类固醇敏感，涉及 II 型糖皮质激素受体。下丘脑 NE 和 5-HT 参与谷氨酸诱导的 HPA 轴激活。
The effect of local administration of glutamate into the hypothalamic paraventricular nucleus (PVN) on the hypothalamo-pituitary adrenocortical (HPA) axis was studied in male rats. Glutamate caused CRH-41 depletion from the median eminence (ME) and a consequent rise in ACTH and corticosterone (CS) serum levels. In rats pretreated with systemic dexamethasone (dex) these effects were completely inhibited. The administration of the glucocorticoid receptor antagonist RU-38486 abolished the inhibitory effect of dex on the adrenocortical discharge. In addition, the depletion of hypothalamic norepinephrine (NE) and serotonin (5-HT) by specific neurotoxins administered into the ventral noradrenergic blundle or into the raphe nuclei respectively, inhibited the response of serum ACTH and CS following PVN glutamate administration. These data indicate that glutamate stimulated the HPA axis via the release of ME CRH-41 into the portal circulation. This response is steroid sensitive involving type II glucocorticoid receptors. Hypothalamic NE and 5-HT participate in the glutamate induced HPA axis activation.