Control of motoneuron function and muscle tone during REM sleep, REM sleep behavior disorder and cataplexy/narcolepsy.
Level 5 - mechanism / opinion, no new human data
Narrative review of preclinical animal and mechanistic research
PubMed 22205591 · doi:10.4449/aib.v149i4.1257
What was done
This narrative review synthesizes research from the author's laboratory examining neurotransmitter systems that regulate somatic motoneuron function and muscle tone during normal REM sleep, REM sleep behavior disorder (RBD), and cataplexy/narcolepsy in transgenic and narcoleptic mouse models.
What was found
The abstract reports no numerical values. It reports qualitatively that: 1) both GABAB and GABAA/glycine-mediated inhibition of motoneurons are required for generating normal REM atonia; 2) impaired GABA and glycine neurotransmission produces cardinal features of RBD in a transgenic mouse model; and 3) loss of excitatory noradrenergic drive to motoneurons contributes to postural muscle tone loss during cataplexy in narcoleptic mice.
Why it matters
The findings identify specific inhibitory and excitatory neurotransmitter pathways underlying normal REM atonia and clinical sleep pathology, highlighting mechanistic targets for RBD and narcolepsy.
Limits
The review relies on rodent models rather than human clinical data, limiting direct translational certainty. The abstract provides no sample sizes, quantitative metrics, or statistical details.
Cited by
- supports Muscle paralysis (atonia) is most pronounced during rapid eye movement (REM) sleep.