Parabrachial and hypothalamic interaction in sodium appetite.

Article date: 2011/7/1

PubMed ID: 322184

Journal name: American journal of physiology. Regulatory, integrative and comparative physiology (ISSN: 1522-1490)

DOI: 10.1152/ajpregu.00615.2010


Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

Author List: Dayawansa S, Peckins S, Ruch S, Norgren R

Publication Types: Journal Article; Research Support, N.I.H., Extramural

Article Date: 2011/01/26

Substances mentioned in the article: Sodium, Dietary;

Mesh terms: Animals; Appetite; Drinking; Eating; Feeding Behavior; Hypothalamus/physiology; Male; Neural Pathways/physiology; Neuroanatomical Tract-Tracing Techniques; Pons/physiology; Rats; Rats, Sprague-Dawley; Sodium, Dietary/administration & dosage; Time Factors; Weight Loss;

Citations: - 2782864

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