Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 2, Pages 411-417Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3115-05.2006
Keywords
aldosterone; ingestive behavior; mineralocorticoid; salt appetite; nucleus of the solitary tract; nucleus tractus solitarius; thirst
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Funding
- NHLBI NIH HHS [R37 HL025449, HL-25449, R01 HL025449] Funding Source: Medline
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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.
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