During REM sleep, the dreaming brain shows vivid hallucinations but the dreamer cannot act them out. Which mechanism specifically suppresses voluntary motor activity during REM sleep?

• A Pontine cholinergic neurons directly hyperpolarise corticospinal neurons in motor cortex layer V, preventing cortical motor output
• B Serotonergic raphe neurons maximally fire during REM, releasing serotonin at neuromuscular junctions to block acetylcholine binding
• C Glutamatergic neurons from the sublaterodorsal nucleus activate spinal interneurons that hyperpolarise alpha motor neurons via glycine and GABA, producing REM atonia ✓
• D Cerebellar Purkinje neurons tonically inhibit deep cerebellar nuclei, preventing all descending motor commands during REM

Explanation

REM sleep atonia is mediated by glutamatergic neurons in the sublaterodorsal/subcoeruleus nucleus (SLD in rodents; equivalent to ventral SLD/precoeruleus in humans) that project to spinal interneurons, which then release glycine and GABA onto alpha motor neurons, causing postsynaptic inhibition and atonia. Failure of this mechanism results in REM sleep behaviour disorder (RBD), where patients act out dreams. Serotonergic raphe neurons are actually silent during REM sleep. Cerebellar Purkinje inhibition affects motor coordination but does not produce the generalised atonia characteristic of REM.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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