Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-7-21
pubmed:abstractText
N-methyl-D-aspartate (NMDA) receptors are widely involved in opioid tolerance. However, it is less clear whether NMDA receptor antagonists reverse already-established tolerance and whether the intensity of the nociceptive stimulus influences morphine tolerance. Three days after implantation of morphine or control pellets the effects of i.v. morphine and pre-administration of saline or (+)-HA966 (a glycine site-specific NMDA receptor antagonist), were studied on the C-fibre reflex elicited by a wide range of stimulus intensities. Morphine both increased the threshold and decreased the slope of the recruitment curve in the "non-tolerant" group of animals. In the "morphine-tolerant" group, the threshold did not change but the gain of the stimulus-response curve decreased. The expression of tolerance to morphine depended on the intensity of the stimulus, being maximal when threshold stimulus intensities were used but considerably less with supra-threshold stimulation. As expected, a single treatment with (+)-HA966, potentiated morphine antinociception in "non-tolerant" rats. However, in "morphine-tolerant" rats (+)-HA966 reversed established morphine tolerance and increased the antinociceptive effects of morphine. These results suggest that (+)-HA966 interfered with expression of morphine tolerance, and offered an encouraging therapeutic approach for pain management in opioid abusers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-202
pubmed:meshHeading
pubmed-meshheading:16713606-Analgesics, Opioid, pubmed-meshheading:16713606-Animals, pubmed-meshheading:16713606-Blood Pressure, pubmed-meshheading:16713606-Drug Tolerance, pubmed-meshheading:16713606-Electric Stimulation, pubmed-meshheading:16713606-Heart Rate, pubmed-meshheading:16713606-Injections, Intravenous, pubmed-meshheading:16713606-Male, pubmed-meshheading:16713606-Morphine, pubmed-meshheading:16713606-Nerve Fibers, Unmyelinated, pubmed-meshheading:16713606-Pain, pubmed-meshheading:16713606-Pain Threshold, pubmed-meshheading:16713606-Pyrrolidinones, pubmed-meshheading:16713606-Rats, pubmed-meshheading:16713606-Rats, Sprague-Dawley, pubmed-meshheading:16713606-Receptors, Glycine, pubmed-meshheading:16713606-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:16713606-Reflex, pubmed-meshheading:16713606-Stereoisomerism, pubmed-meshheading:16713606-Sural Nerve
pubmed:year
2006
pubmed:articleTitle
Tolerance to morphine analgesia: evidence for stimulus intensity as a key factor and complete reversal by a glycine site-specific NMDA antagonist.
pubmed:affiliation
Institut National de la Santé et de la Recherche Médicale (INSERM) U-713, 75013 Paris, France.
pubmed:publicationType
Journal Article