Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control

- GABAergic and MCH neurons of the lateral hypothalamic area control PS.
- Lateral hypothalamic neurons inhibit brainstem PS-off GABAergic neurons.
- Neurons of the pontine sublaterodorsal tegmental nucleus generating PS are glutamatergic.
- The muscle atonia of PS is induced by medullary GABA/glycinergic premotoneurons.

The purpose of this review is to outline our latest hypothesis on the mechanisms responsible for the genesis of paradoxical (REM) sleep (PS). On the basis of recent data, we propose that the onset and maintenance of PS are due to the activation by intrinsic and extrinsic factors of MCH/GABAergic neurons located in the lateral hypothalamic area. These neurons would inhibit during PS, GABAergic PS-off neurons located in the ventrolateral periaqueductal gray region. A number of results strongly suggest that these PS-off neurons gate the activation of the PS-on glutamatergic neurons located in the sublaterodorsal tegmental nucleus (SLD) and responsible for cortical activation and muscle atonia via descending projections to GABA/glycinergic neurons localized in the ventral medullary reticular nuclei.