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脱水诱导的饮水会降低表达血管加压素而非促肾上腺皮质激素释放激素的下丘脑室旁核神经元中的Fos表达。

Dehydration-induced drinking decreases Fos expression in hypothalamic paraventricular neurons expressing vasopressin but not corticotropin-releasing hormone.

作者信息

Wotus Cheryl, Arnhold Michelle M, Engeland William C

机构信息

Department of Neuroscience, Graduate Program in Neuroscience, University of Minnesota, 321 Church Street, Minneapolis, MN 55455, USA.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2007 Mar;292(3):R1349-58. doi: 10.1152/ajpregu.00304.2006. Epub 2006 Oct 26.

DOI:10.1152/ajpregu.00304.2006
PMID:17068162
Abstract

Water-restricted (WR) rats exhibit a rapid suppression of plasma corticosterone following drinking. The present study monitored Fos-like immunoreactivity (Fos) to assess the effect of WR-induced drinking on the activity of vasopressin (VP)-positive magnocellular and parvocellular neurons and corticotropin-releasing hormone (CRH)-positive parvocellular neurons in the paraventricular nucleus of the hypothalamus. Adult male rats received water for 30 min (WR) in the post meridiem (PM) each day for 6 days and were killed without receiving water or at 1 h after receiving water for 15 min. In WR rats, Fos increased in VP magnocellular and parvocellular neurons but not CRH neurons. After drinking, Fos was reduced in VP magnocellular and parvocellular neurons but did not change in CRH neurons. To assess the severity of osmotic stress, rats were sampled throughout the final day of WR. Plasma osmolality, hematocrit and plasma VP were increased throughout the day before PM rehydration, and plasma ACTH and corticosterone were elevated at 1230 and 1430, respectively, showing that WR activates hypothalamic-pituitary-adrenal activity during the early PM before the time of rehydration. To determine the effects of WR-induced drinking on CRH neurons activated by acute stress, WR rats underwent restraint. Restraint increased plasma ACTH and corticosterone and Fos in CRH neurons; although rehydration reduced plasma ACTH and Fos expression in VP neurons, Fos in CRH neurons was not affected. These results suggest that inhibition of VP magnocellular and parvocellular neurons, but not CRH parvocellular neurons, contributes to the suppression of corticosterone after WR-induced drinking.

摘要

限水(WR)大鼠在饮水后血浆皮质酮迅速受到抑制。本研究监测了Fos样免疫反应性(Fos),以评估限水诱导的饮水对下丘脑室旁核中血管加压素(VP)阳性大细胞和小细胞神经元以及促肾上腺皮质激素释放激素(CRH)阳性小细胞神经元活性的影响。成年雄性大鼠每天下午(PM)接受30分钟的水(WR),持续6天,然后在未接受水或接受15分钟水后1小时处死。在限水大鼠中,VP大细胞和小细胞神经元中的Fos增加,但CRH神经元中未增加。饮水后,VP大细胞和小细胞神经元中的Fos减少,但CRH神经元中的Fos没有变化。为了评估渗透应激的严重程度,在限水的最后一天对大鼠进行采样。在下午补液前,血浆渗透压、血细胞比容和血浆VP全天都升高,血浆促肾上腺皮质激素(ACTH)和皮质酮分别在12:30和14:30升高,表明限水在补液前的下午早期激活了下丘脑-垂体-肾上腺活动。为了确定限水诱导的饮水对急性应激激活的CRH神经元的影响,对限水大鼠进行了束缚。束缚增加了血浆ACTH和皮质酮以及CRH神经元中的Fos;尽管补液降低了血浆ACTH和VP神经元中的Fos表达,但CRH神经元中的Fos不受影响。这些结果表明,VP大细胞和小细胞神经元而非CRH小细胞神经元的抑制作用导致了限水诱导饮水后皮质酮的抑制。

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