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This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/R1338    most recent 00391.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Geerling, J. C. Articles by Loewy, A. D. Search for Related Content PubMed PubMed Citation Articles by Geerling, J. C. Articles by Loewy, A. D.

WATER AND ELECTROLYTE HOMEOSTASIS

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst

Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri

Submitted 5 June 2006 ; accepted in final form 21 October 2006

Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11--hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1–4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.

salt appetite; fluid ingestion; hypovolemia; mineralocorticoid; nucleus of the solitary tract

This article has been cited by other articles:

				J. C. Geerling and A. D. Loewy Central regulation of sodium appetite Exp Physiol, February 1, 2008; 93(2): 177 - 209. [Abstract] [Full Text] [PDF]