Aldosterone target neurons in the nucleus tractus solitarius drive sodium appetite
Aldosterone target neurons in the nucleus tractus solitarius drive sodium appetite
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DOI：
10.1523/jneurosci.3115-05.2006
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发表时间：
2006-01-11
影响因子：
5.3
通讯作者：
Loewy, AD
中科院分区：
文献类型：
--
作者：
Geerling, JC;Engeland, WC;Loewy, AD
肾上腺类固醇醛固酮可以通过一种未知的大脑机制增强钠的食欲。孤束核中一组新的神经元表达酶11-β-羟基类固醇脱氢酶2，这使它们对醛固酮有选择性的反应。即使在没有醛固酮的情况下，它们的激活也与钠的食欲在不同的盐分丢失模式中平行。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到的中枢汇聚点，在这个点上，激素和神经信号可以整合起来，驱动钠的胃口。
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.