Inoué S, Honda K, Komoda Y
Institute for Medical and Dental Engineering, Tokyo Medical and Dental University, Japan.
Behav Brain Res. 1995 Jul-Aug;69(1-2):91-6. doi: 10.1016/0166-4328(95)00014-k.
The classical 'hypnotoxin theory' was followed by extensive search for an endogenous sleep substance. Brain tissues and body fluids of sleeping and sleep-deprived animals contained active sleep-inducing factors like the sleep-promoting substance (SPS). Uridine and oxidized glutathione (GSSG), two components of SPS, seem to regulate physiological sleep differentially. Uridine may facilitate the inhibitory neurotransmission at the synaptic level of the GABAA-uridine receptor complex. In contrast, GSSG may inhibit the excitatory neurotransmission at the synaptic level of the glutamate receptor. Thus, the two SPS components promote sleep by exerting a complementary action on the two major neurotransmitter systems in the brain that have mutually reciprocal functions. Further, among multidimensional functions of sleep, uridine may contribute to recover the activity of neurons, while glutathione may counteract excitotoxic events. Hence sleep at the behavioral level is a process of neuronal restitution and detoxification at the cellular level. Such a concept can be regarded as a modern version of the Ishimori-Piéron's hypnotoxin theory proposed early in this century.
继经典的“催眠毒素理论”之后，人们开始广泛寻找内源性睡眠物质。睡眠和睡眠剥夺动物的脑组织和体液中含有活性睡眠诱导因子，如促睡眠物质（SPS）。SPS的两个成分尿苷和氧化型谷胱甘肽（GSSG）似乎对生理性睡眠有不同的调节作用。尿苷可能在GABAA - 尿苷受体复合物的突触水平促进抑制性神经传递。相反，GSSG可能在谷氨酸受体的突触水平抑制兴奋性神经传递。因此，SPS的这两个成分通过对大脑中具有相互反作用的两个主要神经递质系统发挥互补作用来促进睡眠。此外，在睡眠的多维功能中，尿苷可能有助于恢复神经元的活性，而谷胱甘肽可能抵消兴奋性毒性事件。因此，行为水平的睡眠是细胞水平上神经元恢复和解毒的过程。这样的概念可以被视为本世纪初提出的石森 - 皮埃隆催眠毒素理论的现代版本。
