Changes in monoamine release in the ventral horn and hypoglossal nucleus linked to pontine inhibition of muscle tone: an in vivo microdialysis study.
A complete suppression of muscle tone in the postural muscles and a reduction of muscle tone in the respiratory related musculature occur in rapid eye movement (REM) sleep. Previous studies have emphasized the role of glycine in generating these changes. Because the activity of norepinephrine- and serotonin-containing neurons is known to decrease in REM sleep, we hypothesized that a decrease in release in one or both of these transmitters might be detected at the motoneuronal level during muscle tone suppression elicited by brainstem stimulation in the decerebrate animal. We compared release in the ventral horn with that in the hypoglossal nucleus to determine whether the mechanism of muscle tone suppression differs in these nuclei as has been hypothesized. Electrical stimulation and cholinergic agonist injection into the mesopontine reticular formation produced a suppression of tone in the postural and respiratory muscles and simultaneously caused a significant reduction of norepinephrine and serotonin release of similar magnitude in both hypoglossal nucleus and spinal cord. Norepinephrine and serotonin release in the motoneuron pools was unchanged when the stimulation was applied to brainstem areas that did not generate bilateral suppression. No change in dopamine release in the motoneuron pools was seen during mesopontine stimulation-induced atonia. We hypothesize that the reduction of monoamine release that we observe exerts a disfacilitatory effect on both ventral horn and hypoglossal motoneurons and that this disfacilitatory mechanism contributes to the muscle atonia elicited in the decerebrate animal and in the intact animal during REM sleep.
Lai
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YY
Department of Psychiatry and Biobehavioral Neuroscience, School of Medicine, University of California Los Angeles, and Veterans Affairs, Greater Los Angeles Health Care System Medical Center, North Hills, California 91343, USA. yylai@ucla.edu
Kodama
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Siegel
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JM
D000818:Animals; D000870:Anterior Horn Cells / Q000378:metabolism*; D015306:Biogenic Monoamines / Q000378:metabolism*; D002415:Cats; D018679:Cholinergic Agonists / Q000494:pharmacology; D003655:Decerebrate State; D004298:Dopamine / Q000378:metabolism; D004558:Electric Stimulation; D004576:Electromyography; D005260:Female; D007002:Hypoglossal Nerve / Q000378:metabolism*; D008161:Lumbosacral Region; D008297:Male; D008526:Medulla Oblongata / Q000378:metabolism*; D017551:Microdialysis; D009046:Motor Neurons / Q000378:metabolism; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D011149:Pons / Q000187:drug effects / Q000502:physiology*; D012154:Reticular Formation / Q000187:drug effects / Q000502:physiology; D012701:Serotonin / Q000378:metabolism; D013268:Stimulation, Chemical
D015306:Biogenic Monoamines; D018679:Cholinergic Agonists; D012701:Serotonin; D004298:Dopamine; D009638:Norepinephrine