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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-2-23
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pubmed:abstractText |
The nucleus raphe magnus (NRM) is an important descending inhibitory system for pain transmission. We tested whether clonidine, an alpha2-adrenergic agonist, and yohimbine, an alpha2-adrenergic antagonist, modulate the activity of NRM neurons using extracellular recording in a rat brainstem slice preparation. Clonidine 1-20 microM increased firing frequencies (FF) in 22 (37%) and decreased FF in 6 (10%) spontaneously active neurons. Correlation between the concentrations of clonidine and FF changes was unremarkable. Eight spontaneously active neurons (13%) showed increases followed by decreases in FF with increasing doses of clonidine. The remaining 24 neurons (40%) showed no change in FF. Yohimbine 1 microM decreased FF in 38 spontaneously active neurons (58%), whereas the remaining 27 neurons (42%) showed no change in FF. In some neurons, yohimbine antagonized the increase or decrease in FF by application of clonidine. In three silent neurons (25%), clonidine (5 or 10 microM) induced firing activity, which stopped or decreased with the increasing doses of clonidine. In the remaining nine neurons (75%), clonidine did not induce firing activity. We conclude that activation and inhibition of alpha2-adrenergic receptors of NRM neurons augments and suppresses output of the descending inhibitory pain pathway. Implications: The nucleus raphe magnus is implicated in descending control of the nociceptive processes. We found that clonidine and yohimbine increased and decreased, respectively, the firing activity of a substantial number of nucleus raphe magnus neurons. Clonidine and may facilitate and yohimbine may reduce the outflow of the descending inhibitory pathway.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0003-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
88
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
459-61
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:9972774-Adrenergic alpha-Agonists,
pubmed-meshheading:9972774-Adrenergic alpha-Antagonists,
pubmed-meshheading:9972774-Animals,
pubmed-meshheading:9972774-Brain Stem,
pubmed-meshheading:9972774-Clonidine,
pubmed-meshheading:9972774-Dose-Response Relationship, Drug,
pubmed-meshheading:9972774-Neural Inhibition,
pubmed-meshheading:9972774-Neural Pathways,
pubmed-meshheading:9972774-Neurons,
pubmed-meshheading:9972774-Nociceptors,
pubmed-meshheading:9972774-Pain,
pubmed-meshheading:9972774-Raphe Nuclei,
pubmed-meshheading:9972774-Rats,
pubmed-meshheading:9972774-Rats, Wistar,
pubmed-meshheading:9972774-Synaptic Transmission,
pubmed-meshheading:9972774-Yohimbine
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pubmed:year |
1999
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pubmed:articleTitle |
The effect of alpha2-adrenergic drugs on the activity of neurons in the rat nucleus raphe magnus in vitro.
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pubmed:affiliation |
Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, Sapporo, Japan. kantomo@med.hokudai.ac.jp
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pubmed:publicationType |
Journal Article
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