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下丘脑室旁核损伤后大鼠的胃动力和食物摄入量

Gastric motility and food intake in rats after lesions of hypothalamic paraventricular nucleus.

作者信息

Flanagan L M, Dohanics J, Verbalis J G, Stricker E M

机构信息

Department of Behavioral Neuroscience, University of Pittsburgh, Pennsylvania 15260.

出版信息

Am J Physiol. 1992 Jul;263(1 Pt 2):R39-44. doi: 10.1152/ajpregu.1992.263.1.R39.

DOI:10.1152/ajpregu.1992.263.1.R39
PMID:1322067
Abstract

Systemic administration of cholecystokinin (CCK) or LiCl inhibits gastric motility and food intake in rats. Brain stem-projecting oxytocin (OT) neurons in the hypothalamic paraventricular nucleus (PVN) have been proposed to mediate the inhibitory effects of CCK and LiCl on gastric motility and food intake. In the present studies, we found that basal gastric motility was elevated in rats 12-20 h after knife-cut lesions of the PVN; however, this effect disappeared 3 days later. Furthermore, CCK and LiCl inhibited gastric motility at 12-20 h, 3 days, and 3 wk after PVN lesions, although their effects were blunted. Injection of the local anesthetic lidocaine into the PVN had effects similar to acute PVN lesions. In rats with PVN lesions, the inhibitory effects of CCK and LiCl on food intake were indistinguishable from those in sham-lesioned rats. We conclude that the PVN tonically inhibits gastric motility and that it participates in, but is not essential for, the inhibitory effects of CCK and LiCl on gastric motility and food intake in rats.

摘要

胆囊收缩素(CCK)或氯化锂的全身给药可抑制大鼠的胃动力和食物摄入。下丘脑室旁核(PVN)中投射至脑干的催产素(OT)神经元被认为介导了CCK和氯化锂对胃动力和食物摄入的抑制作用。在本研究中,我们发现,PVN切断损伤后12 - 20小时,大鼠的基础胃动力升高;然而,这种效应在3天后消失。此外,CCK和氯化锂在PVN损伤后12 - 20小时、3天和3周时均抑制胃动力,尽管其作用减弱。向PVN注射局部麻醉药利多卡因产生的效应与急性PVN损伤相似。在PVN损伤的大鼠中,CCK和氯化锂对食物摄入的抑制作用与假手术组大鼠无明显差异。我们得出结论,PVN对胃动力具有紧张性抑制作用,并且它参与了CCK和氯化锂对大鼠胃动力和食物摄入的抑制作用,但并非必不可少。

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