Medullary regions mediating atonia.

نویسندگان

  • Y Y Lai
  • J M Siegel
چکیده

Electrical stimulation studies have implicated the medial medulla in the inhibition of muscle tone. In the present report we present evidence for suppression of muscle tone by chemical activation of the medial medulla. We find 2 distinct zones within the classically defined medial medullary inhibitory area. A rostral region corresponding to the nucleus magnocellularis (NMC) is sensitive to glutamate. Atonia produced by activation of this region is mediated by non-NMDA receptors. A caudal region, corresponding to the nucleus paramedianus (NPM) is sensitive to ACh. Atonia produced by activation of this region is mediated by muscarinic receptors. Activation of these regions both in acute decerebrate and intact cats suppresses muscle tone. We find that the cholinoceptive dorsolateral pontine region, previously implicated in atonia control, can be activated by glutamate-sensitive non-NMDA receptors. Microinjection of atropine into the NPM or of glutamylglycine into the NMC blocks atonia elicited by pontine carbachol injection. The medullary regions identified here are hypothesized to mediate the suppression of muscle tone that occurs in rapid eye movement sleep and in cataplexy and may have a role in postural control in waking.

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منابع مشابه

CHOLINERGIC STIMULATION of the rostral part of the pontine reticular formation induces rapid-eye-movement (REM) sleep with atonia in intact animals, and lesions at this pontine site cause REM sleep without atonia.1,2,3 REM sleep without atonia

pontine reticular formation induces rapid-eye-movement (REM) sleep with atonia in intact animals, and lesions at this pontine site cause REM sleep without atonia.1,2,3 REM sleep without atonia is also induced by lesions in the medial medulla.4,5 In the decerebrate cat, both chemical and electrical stimulation delivered to the pontine inhibitory regions, as well as to portions of the medial medu...

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عنوان ژورنال:
  • The Journal of neuroscience : the official journal of the Society for Neuroscience

دوره 8 12  شماره 

صفحات  -

تاریخ انتشار 1988