Francis J, Dourish C T, Cooper S J
Centre for Human Nutrition, University of Sheffield, Northern General Hospital, UK.
Physiol Behav. 1996 Nov;60(5):1337-40. doi: 10.1016/s0031-9384(96)00223-5.
Recently, a number of studies have provided evidence suggesting that CCK and 5-HT interact in the control of food intake. However, the majority of these studies have relied on the administration of exogenous CCK to investigate potential interactions. The aim of the present study was to focus on the potential role of endogenous CCK in 5-HT-CCK interactions. Our prediction was that the CCKA antagonist, devazepide, alone would potentiate the hyperphagic effect of the 5-HT1A agonist, 8-OH-DPAT, in free-feeding rats. The results showed that devazepide, at a dose that had no intrinsic effect (1.0 mg/kg), did not enhance the hyperphagic effect of 8-OH-DPAT (100 and 300 micrograms/kg). This suggests that when serotonergic inhibitory activity is reduced by 5-HT1A-receptor stimulation, there is no compensatory increase of endogenous CCK activity to excite 5-HT neurons and thereby inhibit food intake.
最近，多项研究提供的证据表明，胆囊收缩素（CCK）和5-羟色胺（5-HT）在食物摄入控制方面存在相互作用。然而，这些研究大多依赖于给予外源性CCK来探究潜在的相互作用。本研究的目的是聚焦内源性CCK在5-HT-CCK相互作用中的潜在作用。我们的预测是，胆囊收缩素A（CCKA）拮抗剂地伐西匹单独使用时，会增强5-HT1A激动剂8-羟基二丙胺基四氢萘（8-OH-DPAT）对自由进食大鼠的摄食亢进作用。结果显示，地伐西匹在无内在效应的剂量（1.0毫克/千克）下，并未增强8-OH-DPAT（100和300微克/千克）的摄食亢进作用。这表明，当5-HT1A受体刺激降低血清素能抑制活性时，内源性CCK活性不会代偿性增加以兴奋5-HT神经元，从而抑制食物摄入。
