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胆囊收缩素(CCK)既在中枢神经系统又在胃肠道内存在。据报道,由中枢或外周给予CCK可以在动物和人类引起饱感;但产生这一作用的部位一直有争论。中枢给予CCK-8(CCK羧基端八肽),推测是作用于脑内CCK受体。以前认为外周给予CCK-8通过血循环也作用于大脑,特别是下丘脑腹内侧核区域(简称VMH)。但也有资料报道,损毁大鼠两侧下丘脑VMH区后,由外周给予CCK-8仍可引起饱作用。最近G.P Smith等用大鼠观察了外周给予CCK-8引起饱作用的部位。他们先把大鼠分为两组:一组大鼠毁损两侧下丘脑VMH区;另一组大鼠施行腹腔内迷走神经切除术。然后分别向两组大鼠腹腔内注
Cholecystokinin (CCK) exists both in the central nervous system and in the gastrointestinal tract. It has been reported that central or peripheral administration of CCK can cause satiety in both animals and humans; however, the site that produces this effect has been debated. Central CCK-8 (CCK carboxyl terminal octapeptide), presumably acting on CCK receptors in the brain. CCK-8 was previously thought to act on the brain through the blood circulation, especially in the ventromedial hypothalamic nucleus (VMH). However, there are also data reported that CCK-8 can still cause full-scale administration by damaging the VMH area of the hypothalamus on both sides of the rat. Recently, G.P. Smith et al observed in rats the site of CCK-8-induced satiety in rats. They first divided the rats into two groups: one group of rats that damaged the hypothalamic VMH region on both sides; the other group performed intraperitoneal vagotomy. Then two groups of rats were injected intraperitoneally