下丘脑后部去传入神经支配或5,7-二羟基色胺可抑制光刺激后促肾上腺皮质激素释放激素、促肾上腺皮质激素和皮质酮的反应。

Posterior hypothalamic deafferentation or 5,7-dihydroxytryptamine inhibit corticotropin-releasing hormone, ACTH and corticosterone responses following photic stimulation.

作者信息

Feldman S, Weidenfeld J

机构信息

Department of Neurology, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

出版信息

Neurosci Lett. 1995 Sep 29;198(2):143-5. doi: 10.1016/0304-3940(95)11957-x.

DOI:10.1016/0304-3940(95)11957-x

PMID:8592641

Abstract

The effect of posterior hypothalamic deafferentation (PHD) or hypothalamic serotonin (5-HT) depletion by 5,7-dihydroxytryptamine on corticotropin-releasing hormone (CRH), ACTH and corticosterone (CS) responses, following photic stimulation, was investigated in male rats. In intact animals, photic stimulation caused median eminence (ME) CRH depletion and a rise in serum ACTH and CS levels. In rats with PHD, in which previous studies have demonstrated 5-HT depletion, or with neurotoxin induced hypothalamic 5-HT reduction, these responses were markedly inhibited. This indicates that the blockage in the release of ME CRH into the portal circulation in rats with hypothalamic 5-HT depletion is responsible for the inhibition of the pituitary-adrenocortical responses following photic stimulation.

摘要

在雄性大鼠中，研究了下丘脑后部去传入神经（PHD）或用5,7 - 二羟基色胺使下丘脑5 - 羟色胺（5 - HT）耗竭对光刺激后促肾上腺皮质激素释放激素（CRH）、促肾上腺皮质激素（ACTH）和皮质酮（CS）反应的影响。在完整动物中，光刺激导致正中隆起（ME）CRH耗竭以及血清ACTH和CS水平升高。在先前研究已证明存在5 - HT耗竭的PHD大鼠或神经毒素诱导下丘脑5 - HT减少的大鼠中，这些反应受到明显抑制。这表明下丘脑5 - HT耗竭的大鼠中ME CRH向门脉循环释放受阻是光刺激后垂体 - 肾上腺皮质反应受到抑制的原因。