The neurotransmitter most responsible for the loss of muscle tone (atonia) during REM sleep is:
- A Serotonin withdrawal from raphé nuclei releasing motor neurons from tonic facilitation
- B Norepinephrine released from the locus coeruleus causing hyperpolarisation of motor neurons
- C Adenosine accumulation in the ventrolateral preoptic area suppressing motor activity
- D Glycine and GABA acting on spinal motor neurons via descending pathways from the sublaterodorsal nucleus ✓
Explanation
REM atonia results from active inhibition of spinal motor neurons by descending pathways from the sublaterodorsal nucleus (SLD) in the pons. These pathways excite interneurons in the spinal cord that release glycine and GABA onto alpha motor neurons, causing post-synaptic inhibition and the characteristic flaccid atonia of REM sleep. The withdrawal of norepinephrine and serotonin during REM contributes to reduced arousal but is not the direct mediator of atonia. Failure of this inhibitory pathway leads to REM sleep behaviour disorder. Options B–D are not the primary mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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