期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 622, 期 1-3, 页码 32-36出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2009.09.017
关键词
Arginine-vasopressin; V-1A receptor; Neuropeptide Y; Feeding behavior
资金
- Ministry of Education, Science, and Culture of Japan
- Ministry of Human Health and Welfare of Japan
- Japan Health Sciences Foundation
Food intake is regulated by various factors such as neuropeptide Y. Neuropeptide Y potently induces an increase in food intake, and simultaneously stimulates arginine-vasopressin (AVP) secretion in the brain. Recently, we reported that V-1A vasopressin receptor-deficient (V1AR-/-) mice exhibited altered daily food intake accompanied with hyperglycemia and hyperleptinemia. Here, we further study the involvement of the AVP/V-1A receptor in the appetite regulation of neuropeptide Y with V1AR-/- mice and antagonists for the AVP receptor. The intracerebral-ventricle administration of neuropeptide Y induced greater food consumption in V1AR-/- mice than wild-type (WT) mice, whereas an anorexigenic effect of leptin was not different between the two groups. This finding suggests that the orexigenic effect of neuropeptide Y was enhanced in V1AR-/- mice, leading to the increased food intake in response to the neuropeptide Y stimulation. In addition, the neuropeptide Y-induced orexigenic effect was enhanced by co-administration of OPC-21268, an antagonist for the V-1A vasopressin receptor, into the cerebral ventricle in WT mice, whereas the neuropeptide Y-induced orexigenic effect was not affected by co-administration of SSR-149415, an antagonist for the V-1B vasopressin receptor. These results indicate that AVP could suppress the neuropeptide Y-induced orexigenic effect via the V-1A vasopressin receptor, and that blockade or inhibition of the AVP/V-1A receptor signal resulted in the enhanced neuropeptide Y-induced orexigenic effect Thus, we show that the AVP/V-1A receptor is involved in appetite regulation as an anorexigenic factor for the neuropeptide Y-induced orexigenic effect (C) 2009 Elsevier B.V. All rights reserved.
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