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血管加压素神经元的状态依赖性可塑性:脱水诱导的活动模式变化。

State-dependent plasticity in vasopressin neurones: dehydration-induced changes in activity patterning.

机构信息

Centre for Neuroendocrinology and Department of Physiology, Otago School of Medical Sciences, University of Otago, Dunedin 9054, New Zealand.

出版信息

J Neuroendocrinol. 2010 May;22(5):343-54. doi: 10.1111/j.1365-2826.2010.01961.x. Epub 2010 Jan 19.

Abstract

Moderate dehydration impairs concentration and co-ordination, whereas severe dehydration can cause seizures, brain damage or death. To slow the progression of dehydration until body fluids can be replenished by drinking, the increased body fluid osmolality associated with dehydration increases vasopressin (antidiuretic hormone) secretion from the posterior pituitary gland. Increased vasopressin secretion reduces water loss in the urine by promoting water reabsorption in the collecting ducts of the kidney. Vasopressin secretion is largely determined by action potential discharge in vasopressin neurones, and depends on both the rate and pattern of discharge. Vasopressin neurone activity depends on intrinsic and extrinsic mechanisms. We review recent advances in our understanding of the physiological regulation of vasopressin neurone activity patterning and the mechanisms by which this is altered to cope with the increased secretory demands of dehydration.

摘要

中度脱水会影响注意力和协调性,而严重脱水则会导致癫痫、脑损伤甚至死亡。为了减缓脱水的进程,直到可以通过饮水来补充体液,可以通过增加与脱水相关的体液渗透压来促进垂体后叶分泌血管加压素(抗利尿激素)。增加的血管加压素分泌通过促进肾脏集合管中的水重吸收来减少尿液中的水分流失。血管加压素的分泌在很大程度上取决于血管加压素神经元的动作电位放电,并且取决于放电的速率和模式。血管加压素神经元的活动取决于内在和外在机制。我们回顾了近期在理解血管加压素神经元活动模式的生理调节以及为应对脱水导致的分泌需求增加而改变这些调节机制方面的进展。

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