INSERM, U1028, CNRS, UMR 5292, Lyon Neuroscience Research Center, Team Physiopathologie des réseaux neuronaux responsables du cycle veille-sommeil, Lyon, France.
Pflugers Arch. 2012 Jan;463(1):43-52. doi: 10.1007/s00424-011-1054-y. Epub 2011 Nov 15.
Paradoxical sleep (PS) is characterized by EEG activation with a disappearance of muscle tone and the occurrence of rapid eye movements (REM) in contrast to slow-wave sleep (SWS, also known as non-REM sleep) identified by the presence of delta waves. Soon after the discovery of PS, it was demonstrated that the structures necessary and sufficient for its genesis are restricted to the brainstem. We review here recent results indicating that brainstem glutamatergic and GABAergic, rather than cholinergic and monoaminergic, neurons play a key role in the genesis of PS. We hypothesize that the entrance to PS from SWS is due to the activation of PS-on glutamatergic neurons localized in the pontine sublaterodorsal tegmental nucleus. The activation of these neurons would be due to a permanent glutamatergic input arising from the lateral and ventrolateral periaqueductal gray (vlPAG) and the removal at the onset of PS of a GABAergic inhibition present during W and SWS. Such inhibition would be coming from PS-off GABAergic neurons localized in the vlPAG and the adjacent deep mesencephalic reticular nucleus. The cessation of activity of these PS-off GABAergic neurons at the onset and during PS would be due to direct projections from intermingled GABAergic PS-on neurons. Activation of PS would depend on the reciprocal interactions between the GABAergic PS-on and PS-off neurons, intrinsic cellular and molecular events, and integration of multiple physiological parameters.
异相睡眠（PS）的特点是 EEG 激活伴随着肌肉张力的消失和快速眼动（REM）的发生，与慢波睡眠（SWS，也称为非 REM 睡眠）形成对比，后者的特征是存在 delta 波。PS 发现后不久，就证明了其发生所必需和充分的结构仅限于脑干。我们在这里回顾了最近的结果，表明脑干谷氨酸能和 GABA 能神经元，而不是胆碱能和单胺能神经元，在 PS 的发生中起着关键作用。我们假设从 SWS 进入 PS 是由于位于脑桥 sublaterodorsal 被盖核中的 PS-on 谷氨酸能神经元的激活。这些神经元的激活是由于来自外侧和腹外侧导水管周围灰质（vlPAG）的持续谷氨酸能输入引起的，并且在 PS 开始时去除了在 W 和 SWS 期间存在的 GABA 能抑制。这种抑制来自位于 vlPAG 和相邻深部脑网状核中的 PS-off GABA 能神经元。这些 PS-off GABA 能神经元在 PS 开始和期间活动的停止是由于来自相互混杂的 GABA 能 PS-on 神经元的直接投射。PS 的激活取决于 GABA 能 PS-on 和 PS-off 神经元之间的相互作用、内在的细胞和分子事件以及多个生理参数的整合。
