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REM sleep without atonia after lesions of the medial medulla
1Neurobiology Research, Sepulveda V.A. Medical Center, CA 91343.
Abstract:
Rapid eye movement (REM) sleep is normally accompanied by a complete suppression of tone in the antigravity musculature. Pontine lesions have been shown to block this suppression, producing a syndrome of REM sleep without atonia. We now report that glutamate-induced lesions of the medial medulla, including the nucleus magnocellularis, caudal nucleus gigantocellularis and rostral nucleus paramedianus, produce REM sleep without atonia. These nuclei may function as part of a ponto-medullary system suppressing muscle tone in REM sleep.
Insights
Researchers identified specific brainstem nuclei in the medial medulla that, when lesioned, cause REM sleep without atonia. This suggests these areas are crucial for suppressing muscle tone during REM sleep.
Area of Science:
- Neuroscience
- Sleep Science
Background:
- Rapid eye movement (REM) sleep typically involves muscle atonia.
- Pontine lesions are known to disrupt this muscle tone suppression, causing REM sleep without atonia.
Purpose of the Study:
- To investigate the role of medial medullary nuclei in REM sleep muscle atonia.
- To identify specific brain regions responsible for suppressing muscle tone during REM sleep.
Main Methods:
- Glutamate-induced lesions were performed in the medial medulla.
- Specific nuclei targeted included nucleus magnocellularis, caudal nucleus gigantocellularis, and rostral nucleus paramedianus.
- Muscle tone during REM sleep was assessed in lesioned subjects.
Main Results:
- Lesions in the medial medulla, specifically targeting nucleus magnocellularis, caudal nucleus gigantocellularis, and rostral nucleus paramedianus, resulted in REM sleep without atonia.
- This indicates these nuclei play a role in the muscle tone suppression during REM sleep.
Conclusions:
- The medial medullary nuclei investigated are part of a ponto-medullary system that suppresses muscle tone during REM sleep.
- These findings advance our understanding of the neural circuitry regulating muscle atonia in REM sleep.