During REM sleep, a healthy person experiences complete skeletal muscle atonia except for extraocular muscles and respiratory muscles. The neuroanatomical substrate generating this REM atonia is:

• A Activation of glycinergic and GABAergic neurons in the sublaterodorsal nucleus (SLD) in the pons projecting to spinal ventral horn interneurons ✓
• B Inhibition of motor cortex by thalamocortical loops
• C Withdrawal of orexin input to spinal motor neurons
• D Serotonergic inhibition from raphe nuclei directly on alpha motor neurons

Explanation

REM sleep atonia is mediated by glutamatergic neurons in the sublaterodorsal nucleus (SLD, equivalent to subcoeruleus area) of the pons, which activate glycinergic and GABAergic interneurons in the spinal cord and brainstem ventral horn. These inhibitory interneurons hyperpolarize alpha motor neurons via GABA-A and glycine receptor activation, preventing dream enactment. The atonia spares extraocular muscles (EOMs) because they receive direct pontine control separate from this pathway, and respiratory muscles because premotor breathing circuits (preBötzinger complex) override the atonia. Orexin's role is in arousal-state stabilization, not direct motor neuron inhibition during REM.

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

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