Huber R, Deboer T, Tobler I
Institute of Pharmacology, University of Zürich, Switzerland.
J Sleep Res. 1999 Jun;8 Suppl 1:30-6. doi: 10.1046/j.1365-2869.1999.00006.x.
The prion protein (PrP) is a glycoprotein anchored to cell membranes and expressed in most cell types. Its structural features indicate possible relations to signal peptidases (Glockshuber et al. 1998). Since mutations in this protein lead to severe neurodegeneration and death in humans and animals, it is possible that the loss of its normal function contributes to the development of the pathology. Little is known about its normal function, but there are indications that it may play a role in circadian rhythm and sleep regulation in mice. We explored further whether PrP plays a role in sleep regulation by comparing sleep and the effects of 6 h sleep deprivation in PrP knockout mice and isogenic wild-type mice of the 129/Ola strain. The mice did not differ in the amount and distribution of the vigilance states or in the power spectra. The most remarkable difference was the larger and long-lasting increase of slow-wave activity (mean EEG power density 0.75-4.0 Hz) in non-rapid-eye-movement (NREM) sleep during recovery from sleep deprivation in the null mice. The results confirm our previous findings in mice with a mixed background. This observation applies also to slow-wave activity in NREM sleep episodes following spontaneous waking bouts of different duration. Sleep fragmentation in both genotypes was larger than in mice with the mixed background. A new aspect was revealed by the spectral analysis of the EEG, where the null mice had a lower peak frequency within the theta band in REM sleep and waking, and not in NREM sleep. Behavioural observations concomitant with the EEG indicated that the EEG difference in waking may be attributed to the smaller amount of exploratory behaviour in the null mice. The difference between the genotypes in theta peak frequency was not an overall effect on the EEG, since it was absent in NREM sleep. PrP therefore may be affecting the theta-generating mechanisms in the hippocampus during waking and REM sleep. It remains unresolved whether PrP plays a role in sleep consolidation, nevertheless the data suggest that it is involved in sleep regulation. A passive avoidance test showed a difference between the genotypes. It is not probable that this was due to memory differences, since the genotypes reacted similarly in a delayed T-maze alternation procedure. The behavioural differences need to be pursued further.
朊病毒蛋白(PrP)是一种锚定在细胞膜上的糖蛋白,在大多数细胞类型中都有表达。其结构特征表明它可能与信号肽酶有关(格洛克舒伯等人,1998年)。由于该蛋白的突变会导致人类和动物严重的神经退行性变和死亡,因此其正常功能的丧失可能是导致病理发展的原因。人们对其正常功能知之甚少,但有迹象表明它可能在小鼠的昼夜节律和睡眠调节中发挥作用。我们通过比较PrP基因敲除小鼠和同基因的129/Ola品系野生型小鼠的睡眠情况以及6小时睡眠剥夺的影响,进一步探究PrP是否在睡眠调节中发挥作用。这些小鼠在警觉状态的数量和分布或功率谱方面没有差异。最显著的差异是,在无PrP基因小鼠从睡眠剥夺中恢复期间,非快速眼动(NREM)睡眠中慢波活动(平均脑电图功率密度0.75 - 4.0赫兹)的增加幅度更大且持续时间更长。这些结果证实了我们之前在具有混合背景小鼠中的发现。这一观察结果也适用于不同持续时间的自发清醒发作后NREM睡眠阶段的慢波活动。两种基因型的睡眠片段化程度均大于具有混合背景的小鼠。脑电图的频谱分析揭示了一个新情况,即在快速眼动(REM)睡眠和清醒状态下,无PrP基因小鼠在θ频段内的峰值频率较低,而在NREM睡眠中则不然。与脑电图同步进行的行为观察表明,清醒状态下的脑电图差异可能归因于无PrP基因小鼠的探索性行为较少。θ峰值频率在基因型之间的差异并非对脑电图的整体影响,因为在NREM睡眠中不存在这种差异。因此,PrP可能在清醒和REM睡眠期间影响海马体中θ波的产生机制。PrP是否在睡眠巩固中发挥作用仍未解决,不过数据表明它参与了睡眠调节。一项被动回避测试显示了基因型之间的差异。这不太可能是由于记忆差异,因为在延迟T迷宫交替实验中,两种基因型的反应相似。行为差异需要进一步研究。