Role of the ventromedial hypothalamus in prolactin-induced hyperphagia in ring doves

Citation
Jd. Buntin et al., Role of the ventromedial hypothalamus in prolactin-induced hyperphagia in ring doves, PHYSL BEHAV, 66(2), 1999, pp. 255-261
Citations number
24
Categorie Soggetti
Psycology,"Neurosciences & Behavoir
Journal title
PHYSIOLOGY & BEHAVIOR
ISSN journal
00319384 → ACNP
Volume
66
Issue
2
Year of publication
1999
Pages
255 - 261
Database
ISI
SICI code
0031-9384(199904)66:2<255:ROTVHI>2.0.ZU;2-T
Abstract
Prolactin (PRL) strongly stimulates feeding activity and body weight gain i n ring doves, and of the brain loci tested to date, the ventromedial hypoth alamus (VMH) is the most effective site of PRL action in promoting these ch anges. To determine if the VMH is essential for this response, we examined the effects of VMN destruction on spontaneous feeding and on changes in foo d intake induced by intracerebroventricular (i.c.v.) injections of PRL. Mal e birds were selectively destroyed by radiofrequency lesions (n = 6). A gro up of sham-lesioned males (n = 6) served as controls. Lesioned birds exhibi ted a transient increase in food intake that peaked around the seventh post operative day and declined to baseline levels by day 12. In contrast to thi s pattern, body weights of lesioned birds increased in parallel with food i ntake, but remained elevated throughout the S-week postoperative period. Du ring the peak period of hyperphagia in the lesioned group, food intake and body weight increases were two to three times greater in lesioned birds tha n in controls. After postoperative feed intake had stabilized, each bird re ceived 5 daily i.c.v. injections of ovine PRL. Food intake and body weight increased dramatically in both groups in response to PRL treatment, and no group differences were observed in response to magnitude. We conclude that VMH destruction strongly perturbs feeding and body weight regulation in dov es. However, VMH integrity is not essential for the expression of PRL-induc ed hyperphagia. (C) 1999 Elsevier Science Inc.