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禁水会导致Wistar大鼠和Brattleboro大鼠室旁核神经元以及神经垂体对2-脱氧葡萄糖的摄取增加。

Water deprivation results in increased 2-deoxyglucose uptake by paraventricular neurones as well as pars nervosa in Wistar and Brattleboro rats.

作者信息

Sutherland R C, Martin M J, McQueen J K, Fink G

出版信息

Brain Res. 1983 Jul 18;271(1):101-8. doi: 10.1016/0006-8993(83)91368-9.

DOI:10.1016/0006-8993(83)91368-9
PMID:6883108
Abstract

The [14C]2-deoxyglucose (2-DG) technique has been used in conjunction with quantitative autoradiography to determine the metabolic activity of the neurones of the hypothalamo-neurohypophysial system. Water deprivation (4 days) in Wistar rats led to a more than two-fold increase in the metabolic activity of the pars nervosa (PN), and a significant increase in the metabolic activity of paraventricular (PVN) but not supraoptic (SON) neurones. The PN in homozygous Brattleboro rats was significantly more active than that in hydrated Wistar and Piebald Virol Glaxo (PVG) rats; as in Wistar rats, activity of the PN and PVN was significantly increased by 12-15 h water deprivation. The administration of desamino-D-arginine vasopressin (dDAVP) to Brattleboro rats significantly reduced the activity of the PN to that seen in hydrated Wistar and PVG rats. This reduction in activity was accompanied by a significant reduction in plasma osmolality. These results show that (1) in contrast to studies in which the osmotic stimulus was a salt load, water deprivation leads to a significant increase in 2-DG uptake by the perikarya as well as the terminals of neurohypophysial neurones; (2) increased activity of the neurohypophysial neurones occurs even when there is a genetic deficiency of vasopressin and the activity can be increased further by an osmotic stimulus, and (3) the activity of the neurohypophysial neurones can be significantly reduced by the administration of dDAVP.

摘要

[14C]2-脱氧葡萄糖(2-DG)技术已与定量放射自显影术结合使用,以确定下丘脑-神经垂体系统神经元的代谢活性。对Wistar大鼠进行4天的禁水,导致神经垂体神经部(PN)的代谢活性增加两倍以上,室旁核(PVN)的代谢活性显著增加,但视上核(SON)神经元的代谢活性无显著变化。纯合子布拉特洛伯大鼠的PN活性显著高于水合状态的Wistar大鼠和花斑维尔罗格拉克索(PVG)大鼠;与Wistar大鼠一样,禁水12 - 15小时可使PN和PVN的活性显著增加。给布拉特洛伯大鼠注射去氨基-D-精氨酸血管加压素(dDAVP)可使PN的活性显著降低至水合状态的Wistar大鼠和PVG大鼠的水平。这种活性降低伴随着血浆渗透压的显著降低。这些结果表明:(1)与渗透压刺激为盐负荷的研究相反,禁水导致神经垂体神经元的胞体以及终末对2-DG的摄取显著增加;(2)即使存在血管加压素基因缺陷,神经垂体神经元的活性仍会增加,且渗透压刺激可进一步增强其活性;(3)注射dDAVP可显著降低神经垂体神经元的活性。

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