LICL AND CCK INHIBIT GASTRIC-EMPTYING AND FEEDING AND STIMULATE OT SECRETION IN RATS
LICL AND CCK INHIBIT GASTRIC-EMPTYING AND FEEDING AND STIMULATE OT SECRETION IN RATS
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DOI：
10.1152/ajpregu.1989.256.2.r463
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发表时间：
1989-02-01
影响因子：
--
通讯作者：
STRICKER, EM
中科院分区：
文献类型：
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作者：
MCCANN, MJ;VERBALIS, JG;STRICKER, EM
已知全身注射促性腺激素剂LiCl可增加大鼠神经垂体分泌催产素（OT）。结果表明，催产素的诱导分泌与摄食抑制呈指数关系。在全身注射缩胆囊素（CCK）后，也观察到OT分泌与食物摄入之间的类似关系。然而，每种药剂对食物摄入的影响持续的时间比观察到的OT分泌增加的时间长得多。与此相反，氯化锂和胆囊收缩素产生剂量依赖性抑制胃排空大鼠密切相关的时间抑制的食物摄入。这三个反应的相似性氯化锂和CCK表明，这两种药物刺激共同的中枢机制，显然涉及下丘脑室旁核的大细胞和小细胞神经元，从而这些神经内分泌，行为和自主神经功能的整合。
Systemic injection of the nauseogenic agent LiCl is known to increase neurohypophyseal secretion of oxytocin (OT) in rats. The present results indicated that the induced OT secretion was related exponentially tothe inhibition of food intake. A similar relation between OT secretion and food intake also was observed after systemic injection of the peptide hormone cholecystokinin (CCK). However, the effects of each agent on food intake lasted much longer than the observed increases in OT secretion. In contrast, both LiCl and CCK produced a dose-dependent inhibition of gastric emptying in rats that was closely related temporally to the inhibition of food intake. The similarity of these three responses to LiCl and CCK suggests that both agents stimulate common central mechanisms, apparently involving both magnocellular and parvocellular neurons in the paraventricular nucleus of the hypothalamus, whereby these neuroendocrine, behavioral, and autonomic functions are integrated.