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首页> 外文期刊>American Journal of Physiology >Abdominal vagal mediation of the satiety effects of CCK in rats.
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Abdominal vagal mediation of the satiety effects of CCK in rats.

机译：腹部迷走神经介导CCK对大鼠的饱腹感。

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摘要

CCK type 1 (CCK1) receptor antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCK1 receptors on vagal sensory nerves innervating the small intestine. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of N alpha-3-quinolinoyl-D-Glu-N,N-dipentylamide, does not. At dark onset, non-food-deprived control rats and rats with subdiaphragmatic vagotomies received a bolus injection of devazepide (2.5 micromol/kg i.v.) or a 3-h infusion of A-70104 (3 micromol.kg(-1).h(-1) i.v.) either alone or coadministered with a 2-h intragastric infusion of peptone (0.75 or 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. In control rats both antagonists stimulated food intake and attenuated the anorexic response to intragastric infusion of peptone. In contrast, only devazepide was effective in stimulating food intake in vagotomized rats. Thus endogenous CCK appears to act both at CCK1 receptors beyond the blood-brain barrier and by a CCK1 receptor-mediated mechanism involving abdominal vagal nerves to inhibit food intake.
机译：使用CCK 1型（CCK1）受体拮抗剂在血脑屏障通透性方面的差异来检验以下假设，即饱食感是由CCK1对支配小肠的迷走感觉神经上CCK1受体的作用介导的。地塞哌肽穿透血脑屏障; N-α-3-喹啉基-D-Glu-N，N-二戊酰胺的二环己基铵盐A-70104没有。在黑暗发作时，非食物匮乏的对照大鼠和dia肌下切断术的大鼠接受推注安定肽（2.5 micromol / kg iv）或3小时输注A-70104（3 micromol.kg（-1）.h） （-1）iv）单独或与胃内2小时蛋白ept（0.75或1g / h）共同给药。根据连续的计算机记录食物碗重量的变化来确定食物的摄入量。在对照大鼠中，两种拮抗剂均刺激食物摄入并减弱对胃内输注蛋白ept的厌食反应。相比之下，只有脱氮表肽可有效刺激迷走大鼠的食物摄入。因此，内源性CCK似乎同时作用于血脑屏障以外的CCK1受体，并通过涉及腹部迷走神经的CCK1受体介导的机制来抑制食物摄入。

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