Gottesmann Claude
Laboratoire de Neurobiologie Comportementale, Faculté des Sciences, Université de Nice-Sophia Antipolis, 06108 Nice cedex 2, France.
Brain Res Brain Res Rev. 2004 Jul;45(3):230-49. doi: 10.1016/j.brainresrev.2004.04.003.
Brain function is supported by central activating processes that are significant during waking, decrease during slow wave sleep following waking and increase again during paradoxical sleep during which brain activation is as high as, or higher than, during waking in nearly all structures. However, inhibitory mechanisms are crucial for sleep onset. They were first identified by behavioral, neuroanatomical and electrophysiological criteria, then by pharmacological and neurochemical ones. During slow wave sleep, they are supported by GABAergic mechanisms located at midbrain, mesopontine and pontine levels but are induced and sustained by forebrain and hindbrain influences. GABAergic processes are also responsible for paradoxical sleep occurrence, particularly by suppression of noradrenaline and serotonin (5-HT) inhibition of paradoxical sleep-generating structures. Hindbrain and forebrain modulate these structures situated at the mesopontine level. For sleep mentation, the noradrenergic and serotonergic silence is thought, today, to be directly, or indirectly, responsible for dopamine predominance and glutamate decrease in the nucleus accumbens, which could be the background of the well-known psychotic-like mental activity of dreaming.
大脑功能由中枢激活过程支持，这些过程在清醒时很重要，在清醒后的慢波睡眠期间减少，在异相睡眠期间再次增加，在此期间，几乎所有结构中的大脑激活程度与清醒时一样高或更高。然而，抑制机制对睡眠开始至关重要。它们首先通过行为、神经解剖学和电生理标准被识别，然后通过药理学和神经化学标准被识别。在慢波睡眠期间，它们由位于中脑、脑桥中脑和脑桥水平的GABA能机制支持，但由前脑和后脑的影响诱导并维持。GABA能过程也负责异相睡眠的发生，特别是通过抑制去甲肾上腺素和5-羟色胺（5-HT）对异相睡眠产生结构的抑制。后脑和前脑调节位于脑桥中脑水平的这些结构。对于睡眠思维，如今认为去甲肾上腺素能和5-羟色胺能的沉默直接或间接地导致伏隔核中多巴胺占主导和谷氨酸减少，这可能是做梦时众所周知的类似精神病的精神活动的背景。
