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冷应激和促肾上腺皮质激素释放激素诱导大鼠垂体前叶及富集促肾上腺皮质激素细胞群中L型Ca(2+)通道α(1)亚基信使核糖核酸的变化。

Cold stress and corticotropin-releasing hormone induced changes in messenger ribonucleic acid for the alpha(1)-subunit of the L-type Ca(2+) channel in the rat anterior pituitary and enriched populations of corticotropes.

作者信息

Xie J, Nagle G T, Ritchie A K, Collins T J, Childs G V

机构信息

Department of Anatomy, University of Texas Medical Branch at Galveston, Galveston, Tex., USA.

出版信息

Neuroendocrinology. 1999 Jul;70(1):10-9. doi: 10.1159/000054455.

DOI:10.1159/000054455
PMID:10420089
Abstract

In response to stress, adrenocorticotropin (ACTH) is secreted from anterior pituitary corticotropes. Corticotropin-releasing hormone (CRH) is a potent stimulator of ACTH secretion. The CRH stimulation of secretion is mediated by cAMP and is largely dependent on Ca(2+) influx through voltage-gated L-type Ca(2+) channels. This study was designed to investigate whether the expression of L-type Ca(2+) channels in the rat anterior pituitary and in corticotropes is regulated by acute stress and CRH. RNase protection assays were used to quantify alpha(1C) mRNA of the L-type Ca(2+) channel. The alpha(1C) mRNA levels from stressed rats increased by 31% in anterior pituitaries of rats after 30 min of exposure to cold stress. Neither 60 min cold stress nor 30 min restraint stress had an effect on alpha(1C) mRNA levels. When alpha(1C) mRNA was detected by in situ hybridization in a population of corticotropes enriched to 90%, 0.5 nM CRH (3 h) stimulated a 36% increase in the average area of label/cell and a 10% increase in the average density of label. Our results suggest that (1) the expression of alpha(1C) subunit mRNA of L-type Ca(2+) channels is increased in the rat anterior pituitary with a stress-specific response that might reflect an increase both in thyrotropes and corticotropes (both are known to be stimulated by cold stress), and (2) the CRH-mediated increase in alpha(1C) mRNA expression in individual rat corticotropes, in vitro, supports the hypothesis that some of the increase in vivo is due to changes in corticotropes.

摘要

作为对应激的反应,促肾上腺皮质激素(ACTH)从前垂体促肾上腺皮质激素细胞分泌。促肾上腺皮质激素释放激素(CRH)是ACTH分泌的有效刺激物。CRH对分泌的刺激由cAMP介导,并且在很大程度上依赖于通过电压门控L型Ca(2+)通道的Ca(2+)内流。本研究旨在调查大鼠前垂体和促肾上腺皮质激素细胞中L型Ca(2+)通道的表达是否受急性应激和CRH的调节。采用核糖核酸酶保护试验来定量L型Ca(2+)通道的α(1C) mRNA。暴露于冷应激30分钟后,应激大鼠前垂体中的α(1C) mRNA水平增加了31%。60分钟的冷应激和30分钟的束缚应激均未对α(1C) mRNA水平产生影响。当通过原位杂交在富集至90%的促肾上腺皮质激素细胞群体中检测α(1C) mRNA时,0.5 nM CRH(3小时)刺激标记/细胞的平均面积增加36%,标记的平均密度增加10%。我们的结果表明:(1)L型Ca(2+)通道α(1C)亚基mRNA的表达在大鼠前垂体中因应激特异性反应而增加,这可能反映了促甲状腺激素细胞和促肾上腺皮质激素细胞(两者均已知受冷应激刺激)的增加;(2)体外实验中,CRH介导的大鼠单个促肾上腺皮质激素细胞中α(1C) mRNA表达增加,支持了体内部分增加是由于促肾上腺皮质激素细胞变化的假说。

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