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

Abstract 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...

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Bibliographic Details
Published in:Physiology & behavior 2015-03, Vol.140, p.172-179
Main Authors: Grigson, P.S, Colechio, E.M, Power, M.L, Schulkin, J, Norgren, R
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Appetite - drug effects
Calcium - deficiency
Calcium Chloride - administration & dosage
Calcium depletion
Conditioning (Psychology) - drug effects
Desoxycorticosterone Acetate - pharmacology
Disease Models, Animal
Diuretics - pharmacology
Excitatory Amino Acid Agonists - toxicity
Furosemide - pharmacology
Ibotenic Acid - toxicity
Mineral appetite
Parabrachial
Parabrachial Nucleus - injuries
Parabrachial Nucleus - physiology
Polyethylene Glycols
Psychiatry
Rats
Rats, Sprague-Dawley
Sodium Chloride - administration & dosage
Sodium depletion
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Summary:Abstract 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.
ISSN:0031-9384
1873-507X
DOI:10.1016/j.physbeh.2014.11.070