EVIDENCE OF A PHYSIOLOGICAL-ROLE FOR NEUROPEPTIDE-Y IN VENTROMEDIAL HYPOTHALAMIC LESION-INDUCED HYPERPHAGIA

被引:46
作者
DUBE, MG
KALRA, PS
CROWLEY, WR
KALRA, SP
机构
[1] UNIV FLORIDA,COLL MED,DEPT NEUROSCI,GAINESVILLE,FL 32610
[2] UNIV FLORIDA,COLL MED,DEPT PHYSIOL,GAINESVILLE,FL 32610
[3] UNIV TENNESSEE,COLL MED,DEPT PHARMACOL,MEMPHIS,TN 38163
关键词
NEUROPEPTIDE Y; HYPERPHAGIA; VMH LESION; IMMUNONEUTRALIZATION;
D O I
10.1016/0006-8993(95)00644-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:275 / 278
页数:4
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