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-β-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.
Original language | English (US) |
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Pages (from-to) | 411-417 |
Number of pages | 7 |
Journal | Journal of Neuroscience |
Volume | 26 |
Issue number | 2 |
DOIs | |
State | Published - Jan 11 2006 |
Externally published | Yes |
Keywords
- Aldosterone
- Ingestive behavior
- Mineralocorticoid
- Nucleus of the solitary tract
- Nucleus tractus solitarius
- Salt appetite
- Thirst