REM Sleep–like Atonia of Hypoglossal (XII) Motoneurons Is Caused by Loss of Noradrenergic and Serotonergic Inputs

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Key Points

Determine the role of noradrenergic and serotonergic inputs in REM sleep-like atonia of hypoglossal motoneurons.
Elicited REM sleep-like episodes in anesthetized rats using pontine carbachol injections.
Microinjected prazosin and methysergide into the XII nucleus to assess their effects on motoneuron activity.
Measured spontaneous XII nerve activity before and after antagonism of aminergic receptors.
XII nerve activity reduced by 35 to 81% with antagonists, indicating a role for both neurotransmitters.
Carbachol did not further depress XII nerve activity after antagonists were administered.
Partial recovery of nerve activity was observed, correlating with the withdrawal of antagonists.

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Reveals that noradrenergic and serotonergic antagonism abolishes REM sleep-like atonia in rats, suggesting new therapeutic avenues.

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Fenik et al. (2005) studied this question.

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