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下丘脑室旁核损伤会抑制乙醚诱导的促肾上腺皮质激素释放,但不会抑制催乳素释放。

Lesioning of the hypothalamic paraventricular nucleus inhibits ether-induced ACTH but not prolactin release.

作者信息

Makara G B, Kovács K J

机构信息

Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.

出版信息

Neurobiology (Bp). 1997;5(3):403-11.

PMID:9503384
Abstract

Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.

摘要

应激介质促肾上腺皮质激素释放因子 -41(CRF-41)和加压素已知在下丘脑室旁核(PVN)的小细胞神经分泌神经元中合成并释放,它们对于应激反应时释放促肾上腺皮质激素(ACTH)至关重要。此外,哺乳诱导的催乳素(PRL)释放也依赖于PVN的完整性。在本研究中,对雄性大鼠下丘脑室旁核(PVN)进行损伤后2天、5天和42天,研究了乙醚应激诱导的促肾上腺皮质激素(ACTH)和催乳素(PRL)释放情况。损伤后2天和5天,乙醚诱导的ACTH分泌受到强烈抑制,而6周后损伤诱导的抑制作用逐渐减弱。相反,在研究的任何时间,PVN损伤均未能抑制乙醚诱导的PRL释放。结果表明,与先前的观点相反,应激诱导PRL释放所必需的肽能神经元不在PVN内。

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