Depoortere H, De Saint-Hilaire Z, Nicolaïdis S
Synthelabo Recherche (L.E.R.S.), Bagneux, France.
Physiol Behav. 1990 Dec;48(6):873-7. doi: 10.1016/0031-9384(90)90242-v.
EEG sleep recordings were performed in rats after administration of CCK-8. Mildly food-deprived rats were given IP CCK-8 (8 and 16 micrograms/kg body weight) and behavioural as well as EEG changes were examined. With 16 micrograms/kg of CCK-8, there was a significant increase of slow wave sleep in the 30 min of recording. Paradoxical sleep was unchanged or slightly decreased. The low dose of CCK-8 did not promote sleep. In addition both doses of CCK-8 induced EEG alterations including the presence of unusual acute spikes and slowing of EEG rhythm concomitant with awake immobility in rats. The computerized spectral analysis showed that CCK-8 slowed the EEG-wave frequency without modifying the total power energy in comparison with control wakefulness. In contrast, there was no effect in alcuronium-immobilized rats after 8 to 32 micrograms/kg IP of CCK-8. These observations do not support the idea that CCK-8, as a satiating factor like food, would promote sleep.
在给予大鼠CCK - 8后进行脑电图睡眠记录。轻度食物剥夺的大鼠腹腔注射CCK - 8（8微克/千克体重和16微克/千克体重），并检查行为和脑电图变化。给予16微克/千克的CCK - 8后，记录的30分钟内慢波睡眠显著增加。异相睡眠未改变或略有减少。低剂量的CCK - 8不促进睡眠。此外，两种剂量的CCK - 8均诱导脑电图改变，包括出现异常急性尖波和脑电图节律减慢，同时伴有大鼠清醒不动。计算机频谱分析表明，与对照清醒状态相比，CCK - 8减慢了脑电图波频率，但未改变总能量。相反，腹腔注射8至32微克/千克CCK - 8后，对用阿库氯铵固定的大鼠没有影响。这些观察结果不支持CCK - 8作为一种像食物一样的饱腹感因子会促进睡眠的观点。
