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rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-1-4
pubmed:abstractText
The authors sought to investigate the role of a common single nucleotide polymorphism in the mu-opioid receptor gene (OPRM1) 118A > G for nociceptive sensory processing using event-related potentials (ERPs). Specific nociceptive (carbon dioxide [CO-sub-2]: 40% volume-to-volume [vol/vol] and 60% vol/vol) and nonnociceptive (hydrogen sulfide, 2 parts per million [ppm] and 4 ppm) stimuli were applied to the nasal mucosa of 45 volunteers. ERPs were recorded from a central lead. In this random sample, we found 37 noncarriers, 7 heterozygous carriers, and 1 homozygous carrier of the variant OPRM1 118G allele (allelic frequency, 10%). Amplitudes of nociceptive ERP in carriers of this allele were, on average, half as high as those of noncarriers. In discriminant analysis, ERP amplitude N1 response to the weaker nociceptive stimuli was the only ERP parameter that discriminated statistically significantly between carriers and noncarriers of the variant 118G allele. On the basis of N1-CO-sub-2 (40% vol/vol), the authors correctly backclassified 68.6% of the cases as carriers or noncarriers of the allele. The OPRM1 118A > G polymorphism specifically modulates nociceptive but not nonnociceptive cortical activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0735-7044
pubmed:author
pubmed:copyrightInfo
2006 APA, all rights reserved
pubmed:issnType
Print
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1218-24
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
The human mu-opioid receptor gene polymorphism 118A > G decreases cortical activation in response to specific nociceptive stimulation.
pubmed:affiliation
pharmazentrum frankfurt/ZAFES, Institute of Clinical Pharmacology, Johann Wolfgang Goethe University, Frankfurt am Main, Germany.
pubmed:publicationType
Journal Article