Neural Control of REM Sleep and Motor Atonia: Current Perspectives.
Level 5 - mechanism / opinion, no new human data
Narrative review of preclinical and mechanistic animal studies
PubMed 38060134 · doi:10.1007/s11910-023-01322-x
What was done
This narrative review summarizes literature on the neuronal populations, synaptic mechanisms, and circuit architectures regulating rapid eye movement (REM) sleep and motor atonia, emphasizing recent findings from conditional genetic manipulation studies in rodent models.
What was found
The abstract reports no numerical data. Qualitatively, it highlights that glutamatergic neurons in the sublaterodorsal nucleus (SLD_Glut) serve as essential primary generators for REM sleep, orchestrating cortical activation, hippocampal activation, and muscle atonia via distinct pathways. Damage to these neurons or their descending atonia pathways produces REM sleep behavior disorder, whereas abnormal wake-state activation of this circuitry is linked to cataplexy in narcolepsy.
Why it matters
It clarifies the central pontine circuitry controlling REM sleep features and provides a mechanistic framework linking specific neuronal subpopulation dysfunctions to clinical sleep pathologies such as REM behavior disorder and narcolepsy.
Limits
The review relies primarily on rodent neurobiological models, limiting direct translation to human physiology without clinical validation. The abstract does not report systematic review methodology, study selection criteria, or quantitative data, and notes ongoing debate regarding alternative models of REM sleep generation.