Currie P J, Coscina D V
Department of Psychology, Wayne State University, Detroit, MI 48202, USA.
Neuroreport. 1995 Dec 29;7(1):253-6.
Several recent studies have suggested that feeding suppression is mediated jointly by enhanced neurotransmission of cholecystokinin (CCK) and serotonergic (5-HT) systems. In the present study the CCKA receptor antagonist devazepide (50-200 micrograms kg-1, s.c.) was found reliably to potentiate the feeding response elicited by dorsal or median raphe injection of the 5-HT1A agonist 8-OH-DPAT (0.2-0.8 nmol). This effect was evident following co-administration of both feeding threshold and subthreshold doses of either compound, suggesting that the simultaneous suppression of CCK and 5-HT function may interact as joint effectors of overeating.
最近的几项研究表明，进食抑制是由胆囊收缩素（CCK）和血清素能（5-HT）系统增强的神经传递共同介导的。在本研究中，发现CCKA受体拮抗剂地伐西匹（50 - 200微克/千克，皮下注射）能可靠地增强由中缝背核或中缝正中核注射5-HT1A激动剂8-羟基二丙胺基四氢萘（0.2 - 0.8纳摩尔）所引发的进食反应。在同时给予两种化合物的进食阈值剂量和阈下剂量后，这种效应很明显，这表明CCK和5-HT功能的同时抑制可能作为暴饮暴食的联合效应器相互作用。
