Tsai S H, Passaro E, Lin M T
Neuropharmacology. 1984 Nov;23(11):1351-6. doi: 10.1016/0028-3908(84)90059-5.
Administration of cholecystokinin (CCK) (0.2 - 0.6 micrograms in a volume of 2 microliter) into the lateral cerebral ventricle caused a decrease in intake of food but a relative increase in intake of water (or water-to-food ratio) in rats. To determine whether the anorexic actions of CCK were mediated through the hypothalamic nuclei, rats were infused with CCK (0.02 - 0.12 microgram in a volume of 0.5 microliter) through previously implanted hypothalamic cannulae. Administration of CCK into the lateral hypothalamus, but not the anterior hypothalamus or ventromedial hypothalamus, caused decreased intake of food and a relative increased intake of water. In addition, the responses induced by injection of CCK into the hypothalamus were completely abolished by selective depletion of catecholamines in the hypothalamus (eg. noradrenaline and dopamine) with intra-hypothalamic injection of 6-hydroxydopamine. Intraperitoneal administration of 0.12 microgram of CCK had no effect on the intake of food and water in rats. The data indicate that CCK acts through catecholaminergic mechanisms in the hypothalamus to influence feeding behaviour.
向大鼠侧脑室注射胆囊收缩素(CCK)(0.2 - 0.6微克,体积为2微升)会导致食物摄入量减少,但水摄入量(或水与食物的比例)相对增加。为了确定CCK的厌食作用是否通过下丘脑核介导,通过先前植入的下丘脑套管向大鼠注入CCK(0.02 - 0.12微克,体积为0.5微升)。向外侧下丘脑而非前下丘脑或腹内侧下丘脑注射CCK会导致食物摄入量减少和水摄入量相对增加。此外,通过下丘脑内注射6 - 羟基多巴胺选择性耗尽下丘脑内的儿茶酚胺(如去甲肾上腺素和多巴胺)后,向下丘脑注射CCK所诱导的反应完全消失。腹腔注射0.12微克CCK对大鼠的食物和水摄入量没有影响。数据表明,CCK通过下丘脑内的儿茶酚胺能机制影响进食行为。