Cox J E, Brown P T, Toney R J, Wiebe D J
Behav Brain Res. 1984 Oct;14(1):41-50. doi: 10.1016/0166-4328(84)90018-4.
We compared changes in runway performance by rats for sucrose reward following injections of the synthetic C-terminal octapeptide of cholecystokinin (CCK-8) with those seen after variations in food deprivation and injections of lithium chloride. No effects on running for either 10% or 30% sucrose were found following 0.5 to 4.0 micrograms/kg of CCK-8, though such doses suppressed 30-min sucrose intake up to 53%. Statistically reliable slowing of running for 10% sucrose was observed on two series of tests after 8.0 micrograms/kg of CCK-8. Running for 30% sucrose was not significantly affected by this dose. The general ineffectiveness of CCK-8 for producing decrements in running spread contrasts with significantly reduced performance after either reductions in food deprivation (21 h vs 12 and 3 h) or injections of 75 mg/kg lithium chloride. These results suggest that the mode of action of CCK-8 in reducing food intake is different than that produced by changes in hunger or by non-specific interference with motivation by malaise. The finding that CCK-8 can substantially reduce consumption with no apparent changes in appetitive motivation is consistent with the hypothesis that this substance acts only late in the meal to prematurely trigger satiety.
我们比较了注射胆囊收缩素(CCK-8)的合成C末端八肽后,大鼠为获取蔗糖奖励在跑道上表现的变化,以及在改变食物剥夺程度和注射氯化锂后所观察到的变化。注射0.5至4.0微克/千克的CCK-8后,未发现对大鼠跑向10%或30%蔗糖的行为有任何影响,尽管如此剂量可将30分钟的蔗糖摄入量抑制高达53%。在注射8.0微克/千克的CCK-8后的两组测试中,观察到大鼠跑向10%蔗糖时在统计学上有可靠的速度减慢。此剂量对大鼠跑向30%蔗糖的行为未产生显著影响。CCK-8在使奔跑速度下降方面普遍无效,这与食物剥夺程度降低(21小时与12小时和3小时相比)或注射75毫克/千克氯化锂后表现显著降低形成对比。这些结果表明,CCK-8减少食物摄入的作用方式不同于饥饿变化或不适对动机的非特异性干扰所产生的作用方式。CCK-8能大幅减少摄入量而对食欲动机无明显影响这一发现,与该物质仅在进食后期过早触发饱腹感的假说相符。