Depoortere H
Laboratoires d'Etudes et de Recherches Synthélabo (LERS), Bagneux, France.
Neuropsychobiology. 1987;18(3):160-8. doi: 10.1159/000118411.
In the present study, we investigated the different types of neocortical rhythmic slow activity (RSA) during wakefulness and paradoxical sleep as well as their pharmacological modification. During wakefulness, the high-frequency (7-9 Hz) RSA1 type, which is atropine-resistant, is accentuated by forebrain stimulation and is abolished by urethane, clonidine and alcuronium. These drugs induce the low-frequency (4-6 Hz) RSA2 type that is atropine-sensitive and is activated by cholinergic agents and by some drugs such as tabernanthine, ibogaine, vincamine, SL 76.188-MS (10-chloro-hexahydrocanthinone methanesulphonate). The effects of pilocarpine and SL 76.188-MS on RSA2 are antagonized by atropine and hemicholinium-3, which suggests the involvement of a cholinergic pathway in the neocortical RSA activation (as has been demonstrated for the hippocampal RSA). During paradoxical sleep, two types of RSA are also observed: RSAT, of low frequency (5-7 Hz) present during its tonic components, and RSAp, of high frequency (7-9 Hz) which is well correlated with phasic phenomena such as bursts of rapid eye movements generated, or controlled, by cholinergic mechanisms. Imipramine reduces phasic phenomena and the periods of neocortical RSAp. Alcuronium does not modify RSAp in paradoxical sleep-deprived rats and suppress RSA1 during arousal, observations which would suggest that RSAp and RSA1 are regulated by two distinct central mechanisms. The EEG studies of neocortical RSA during wakefulness and paradoxical sleep allow the selection and the differentiation of pharmacological agents. Furthermore, this approach not only may represent a basis for the treatment of deficits in the regulation of vigilance and memory, but also a novel strategy for the analysis of RSA type of paradoxical sleep with respect to antidepressant and anxiolytic treatment.
在本研究中，我们调查了清醒和异相睡眠期间不同类型的新皮质节律性慢活动（RSA）及其药理学改变。在清醒期间，高频（7 - 9赫兹）的RSA1型对阿托品有抗性，经前脑刺激会增强，而被乌拉坦、可乐定和阿库氯铵消除。这些药物会诱发低频（4 - 6赫兹）的RSA2型，该型对阿托品敏感，且会被胆碱能药物以及某些药物如育亨宾碱、伊博格碱、长春胺、SL 76.188 - MS（10 - 氯 - 六氢坎替酮甲磺酸盐）激活。毛果芸香碱和SL 76.188 - MS对RSA2的作用会被阿托品和半胱氨酸转运体抑制剂3拮抗，这表明胆碱能通路参与了新皮质RSA的激活（正如海马体RSA所证实的那样）。在异相睡眠期间，也观察到两种类型的RSA：RSAT，低频（5 - 7赫兹），出现在其紧张性成分期间；以及RSAp，高频（7 - 9赫兹），与诸如由胆碱能机制产生或控制的快速眼动爆发等相位现象密切相关。丙咪嗪会减少相位现象和新皮质RSAp的持续时间。阿库氯铵在异相睡眠剥夺的大鼠中不会改变RSAp，但在觉醒期间会抑制RSA1，这些观察结果表明RSAp和RSA1由两种不同的中枢机制调节。对清醒和异相睡眠期间新皮质RSA的脑电图研究有助于选择和区分药理学药物。此外，这种方法不仅可能代表治疗警觉和记忆调节缺陷的基础，而且是一种关于抗抑郁和抗焦虑治疗分析异相睡眠RSA类型的新策略。
