Goonawardena Anushka V, Plano Andrea, Robinson Lianne, Platt Bettina, Hampson Robert E, Riedel Gernot
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1083, USA.
Sleep Disord. 2011;2011:178469. doi: 10.1155/2011/178469. Epub 2012 Jan 4.
The plant cannabinoid Δ(9)-tetrahydrocannabinol and the endocannabinoid anandamide increase the amount of sleep via a CB1 receptor mediated mechanism. Here, we explored the use of a novel electroencephalogram (EEG) recording device based on wireless EEG microchip technology (Neurologger) in freely-moving rats, and its utility in experiments of cannabinoids-induced alterations of EEG/vigilance stages. EEG was recorded through epidural electrodes placed above pre-frontal and parietal cortex (overlaying the dorsal hippocampus). As cannabinoids, we acutely administered the full synthetic CB1 receptor agonist, WIN55,212-2 (1 mg/kg), and the antagonist/inverse agonist, AM251 (2 mg/kg), either alone or together through the intraperitoneal route. WIN55,212-2 increased the total amount of NREM sleep and the length of each NREM bout, but this was unlikely due to CB1 receptor activation since it was not prevented by AM251. However, WIN55,212-2 also lowered overall EEG spectral power especially in theta and alpha frequency bands during wakefulness and NREM sleep, and this effect was reversed by AM251. The antagonist/inverse agonist caused no sleep alterations by itself and moderately increased spectral power in Theta, alpha and beta frequency bands during NREM sleep when administered on its own. Implications of endocannabinoid modulation of the sleep-wake cycle and its possible interactions with other transmitter systems are considered.
植物大麻素Δ(9)-四氢大麻酚和内源性大麻素花生四烯乙醇胺通过CB1受体介导的机制增加睡眠时间。在此，我们探索了一种基于无线脑电图微芯片技术（神经记录器）的新型脑电图（EEG）记录设备在自由活动大鼠中的应用，以及其在大麻素诱导的EEG/警觉阶段改变实验中的效用。通过置于前额叶和顶叶皮质上方（覆盖背侧海马体）的硬膜外电极记录EEG。作为大麻素，我们通过腹腔途径单独或联合急性给予全合成CB1受体激动剂WIN55,212-2（1mg/kg）和拮抗剂/反向激动剂AM251（2mg/kg）。WIN55,212-2增加了非快速眼动睡眠的总量和每个非快速眼动睡眠时段的长度，但这不太可能是由于CB1受体激活，因为AM251并不能阻止这种增加。然而，WIN55,212-2还降低了清醒和非快速眼动睡眠期间的总体EEG频谱功率，尤其是在θ和α频段，而AM251可逆转这种效应。拮抗剂/反向激动剂本身不会引起睡眠改变，单独给药时在非快速眼动睡眠期间会适度增加θ、α和β频段的频谱功率。我们考虑了内源性大麻素对睡眠-觉醒周期的调节及其与其他递质系统可能的相互作用的意义。
