孤束核中的醛固酮靶神经元驱动钠食欲。
Aldosterone target neurons in the nucleus tractus solitarius drive sodium appetite.
作者信息
Geerling Joel C, Engeland William C, Kawata Mitsuhiro, Loewy Arthur D
机构信息
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
出版信息
J Neurosci. 2006 Jan 11;26(2):411-7. doi: 10.1523/JNEUROSCI.3115-05.2006.
Abstract
Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-beta-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.
摘要
肾上腺类固醇醛固酮可通过一种未知的脑机制增强钠食欲。孤束核中的一组新型神经元表达2型11-β-羟基类固醇脱氢酶，这使得它们对醛固酮具有选择性反应。即使在没有醛固酮的情况下，它们的激活在不同的失盐模式中与钠食欲平行。这些独特的醛固酮靶神经元可能代表了一个以前未被认识的中枢汇聚点，在这个点上激素和神经信号可以整合起来驱动钠食欲。
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