Parabrachial lesions in rats disrupt sodium appetite induced by furosemide but not by calcium deprivation

PHYSIOLOGY & BEHAVIOR

卷:140

Article

Grigson, P. S.¹  Colechio, E. M.¹  Power, M. L.^2,3  Schulkin, J.⁴  Norgren, R.¹ 

[1] Penn State Univ, Coll Med, Dept Neural & Behav Sci, Hershey, PA 17033 USA

[2] Natl Zool Pk, Nutr Lab, Washington, DC 20013 USA

[3] Natl Zool Pk, Conservat Ecol Ctr, Smithsonian Conservat Biol Inst, Washington, DC 20013 USA

[4] Georgetown Univ, Dept Neurosci, Washington, DC 20057 USA

关键词: Mineral appetite;    Parabrachial;    Calcium depletion;    Sodium depletion;   

DOI  :  10.1016/j.physbeh.2014.11.070

来源: Elsevier

【 摘 要 】

An appetite for CaCl2 and NaCl occurs in young rats after they are fed a diet lacking Ca or Na, respectively. Bilateral lesions of the parabrachial nuclei (PBN) disrupt normal taste aversion learning and essentially eliminate the expression of sodium appetite. Here we tested whether similar lesions of the PBN would disrupt the calcium-deprivation-induced appetite for CaCl2 or NaCl. Controls and rats with PBN lesions failed to exhibit a calcium-deprivation-induced appetite for CaCl2. Nevertheless, both groups did exhibit a significant calcium-deprivation-induced appetite for 0.5 M NaCl. Thus, while damage to the second central gustatory relay in the PBN disrupts the appetite for 0.5 M NaCl induced by furosemide, deoxycorticosterone acetate, and polyethylene glycol, the sodium appetite induced by dietary CaCl2 depletion remains intact. (C) 2015 Elsevier Inc. All rights reserved.

【 授权许可】

Free