Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 300, Issue 5, Pages R1091-R1099Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00615.2010
Keywords
ibotenic acid; lateral hypothalamus; asymmetric lesions; parabrachial nuclei
Categories
Funding
- National Institute on Deafness and Other Communication Disorders [DC-05435, DC-008937]
Ask authors/readers for more resources
Dayawansa S, Peckins S, Ruch S, Norgren R. Parabrachial and hypothalamic interaction in sodium appetite. Am J Physiol Regul Integr Comp Physiol 300: R1091-R1099, 2011. First published January 26, 2011; 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available