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RU-486可阻断应激诱导的大鼠下丘脑室旁核中脑啡肽原基因表达增强。

RU-486 blocks stress-induced enhancement of proenkephalin gene expression in the paraventricular nucleus of rat hypothalamus.

作者信息

García-García L, Harbuz M S, Manzanares J, Lightman S L, Fuentes J A

机构信息

Departamento de Farmacologia, Facultad de Farmacia and Instituto Pluridisciplinar Universidad Complutense, Madrid 28040, Spain.

出版信息

Brain Res. 1998 Mar 9;786(1-2):215-8. doi: 10.1016/s0006-8993(97)01416-9.

DOI:10.1016/s0006-8993(97)01416-9
PMID:9555022
Abstract

The purpose of this study was to investigate the glucocorticoid (GC) mediated regulation of corticotropin-releasing hormone (CRH) and proenkephalin (PE) gene expressions in the paraventricular nucleus (PVN) of the hypothalamus during physical stress induced by a single intraperitoneal (i.p.) injection of hypertonic saline (9% NaCl). Previous intracerebroventricular (i.c.v.) administration of the type II glucocorticoid receptor (GR) antagonist RU-486 (20 ng/rat), increased the basal CRH mRNA levels in the PVN but had no effect on PE gene expression. Stress induced by injection of hypertonic saline increased both CRH and PE mRNA levels in PVN. Administration of RU-486 completely blocked the stress-induced increase of PE mRNA levels, but failed to alter the CRH mRNA levels in the PNV. These data suggests that, under these experimental conditions, endogenous GC are necessary for a normal PE response to hypertonic saline stress.

摘要

本研究的目的是调查在单次腹腔注射高渗盐水(9%氯化钠)诱导的身体应激期间,糖皮质激素(GC)对下丘脑室旁核(PVN)中促肾上腺皮质激素释放激素(CRH)和前脑啡肽(PE)基因表达的调节作用。先前经脑室注射II型糖皮质激素受体(GR)拮抗剂RU - 486(20 ng/大鼠)可增加PVN中基础CRH mRNA水平,但对PE基因表达无影响。注射高渗盐水诱导的应激增加了PVN中CRH和PE mRNA水平。给予RU - 486完全阻断了应激诱导的PE mRNA水平升高,但未能改变PNV中CRH mRNA水平。这些数据表明,在这些实验条件下,内源性GC对于正常的PE对高渗盐水应激反应是必需的。

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