The atonia of skeletal muscles during REM sleep is generated by active inhibition of motor neurons. The neural pathway responsible involves:

• A Reticular activating system (RAS) directly inhibiting anterior horn cells via the corticospinal tract
• B Adenosine accumulation during REM selectively binding to motor neuron A1 receptors
• C Pontine REM-on neurons (subcoeruleus nucleus) activating medullary inhibitory neurons that release glycine and GABA onto spinal motor neurons ✓
• D Reduced acetylcholine at the neuromuscular junction during REM due to pontine cholinergic withdrawal

Explanation

REM sleep atonia is an active inhibitory process, not passive cessation of motor drive. The subcoeruleus nucleus (SLC/peri-locus coeruleus alpha) in the pons contains glutamatergic 'REM-on' neurons that project to the ventromedial medullary reticular formation. These medullary neurons in turn project to spinal cord ventral horn motor neurons, releasing glycine (hyperpolarizing inhibition) and GABA. Loss of this pathway (e.g., pontine lesions) causes REM sleep behavior disorder (RBD) where patients physically act out dreams. Adenosine primarily regulates sleep drive (homeostatic), not atonia specifically.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.