Which structure generates paradoxical (REM) sleep: The brainstem, the hypothalamus, the amygdala or the cortex?
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and neuroanatomical circuitry without systematic search criteria or primary human data.
PubMed 38422648 · doi:10.1016/j.smrv.2024.101907
What was done
This narrative review synthesized evidence regarding the contributions of brainstem, hypothalamic, amygdalar, and cortical structures to the generation and maintenance of paradoxical sleep (PS/REM sleep).
What was found
The abstract reports no numerical data. Mechanistically, the authors propose that PS muscle atonia is mediated by pontine sublaterodorsal tegmental nucleus (SLD) glutamatergic neurons projecting to glycinergic/GABAergic premotor neurons in the ventromedial medulla. SLD PS-on neurons are suppressed during wakefulness and slow-wave sleep by ventrolateral periaqueductal gray and deep mesencephalic reticular nucleus GABAergic PS-off neurons. Melanin-concentrating hormone and GABAergic PS-on neurons in the posterior hypothalamus inhibit these PS-off neurons to initiate PS. Limbic cortical activation (via the claustrum and supramammillary nucleus) and the basolateral amygdala further modulate PS expression and memory consolidation.
Why it matters
It outlines an integrated neuroanatomical model of REM sleep generation spanning brainstem executive centers, hypothalamic switches, and forebrain memory circuits.
Limits
The abstract describes a narrative conceptual model without systematic search criteria, quantitative meta-analysis, or primary human clinical trials. Most underlying neurocircuitry data derive from preclinical animal preparations.