Evidence of a physiological role for neuropeptide Y in ventromedial hypothalamic lesion-induced hyperphagia.
We evaluated the role of neuropeptide Y (NPY), a potent endogenous orexigenic signal, in the ventromedial hypothalamic (VMH) lesion-induced hyperphagia in rats. To produce hyperphagia and excessive weight gain, adult female rats received bilateral electrolytic or sham lesions in the VMH. Concurrently, a permanent intracerebroventricular cannula was implanted in the third ventricle of the brain. After a recovery period, these rats were passively immunized against NPY to evaluate the role of endogenous NPY on hyperphagia. The results showed that intraventricular administration of NPY antibodies abolished the hyperphagia in VMH-lesioned rats. These revelations are in agreement with the notion that altered hypothalamic NPY release or action may underlie the hyperphagia and excessive weight gain seen in response to structural damage in the VMH.
Dube
M G
MG
Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610-0244, USA.
Kalra
P S
PS
Crowley
W R
WR
Kalra
S P
SP
D000818:Animals; D004558:Electric Stimulation; D005260:Female; D006963:Hyperphagia / Q000503:physiopathology*; D007033:Hypothalamus, Middle / Q000502:physiology*; D007116:Immunization, Passive; D007276:Injections, Intraventricular; D009478:Neuropeptide Y / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015430:Weight Gain
D009478:Neuropeptide Y