The VPAC2 receptor is essential for circadian function in the mouse suprachiasmatic nuclei

被引：446
作者：
Harmar, AJ
Marston, HM
Shen, SB
Spratt, C
West, KM
Sheward, WJ
Morrison, CF
Dorin, JR
Piggins, HD
Reubi, JC
Kelly, JS
Maywood, ES
Hastings, MH
机构：
[1] Univ Edinburgh, Dept Neurosci, Edinburgh EH8 9JZ, Midlothian, Scotland
[2] Univ Edinburgh, Fujisawa Inst Neurosci, Edinburgh EH8 9JZ, Midlothian, Scotland
[3] Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland
[4] Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England
[5] Univ Bern, Inst Pathol, CH-3010 Bern, Switzerland
[6] MRC, Mol Biol Lab, Cambridge CB2 2QH, England
来源：
CELL | 2002年 / 109卷 / 04期
基金：
英国惠康基金; 英国医学研究理事会;
关键词：
D O I：
10.1016/S0092-8674(02)00736-5
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The neuropeptides pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are implicated in the photic entrainment of circadian rhythms in the suprachiasmatic nuclei (SON). We now report that mice carrying a null mutation of the VPAC(2) receptor for VIP and PACAP(Vipr2(-/-)) are incapable of sustaining normal circadian rhythms of rest/activity behavior. These mice also fail to exhibit circadian expression of the core clock genes mPer1, mPer2, and mCry1 and the clock-controlled gene arginine vasopressin (AVP) in the SON. Moreover, the mutants fail to show acute induction of mPer1 and mPer2 by nocturnal illumination. This study highlights the role of intercellular neuropeptidergic signaling in maintenance of circadian function within the SCN.
引用
收藏
页码：497 / 508
页数：12
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