Source:http://linkedlifedata.com/resource/pubmed/id/16123758
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| Predicate | Object |
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| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2005-12-16
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| pubmed:abstractText |
A polymorphism in the mu-opioid receptor (MOR) (A118G) has been shown to increase beta-endorphin binding affinity, theoretically placing greater inhibitory tone on hypothalamic corticotropin-releasing hormone (CRH) neurons. We hypothesized that the minor allele (G) would predict cortisol responses to both pharmacological (naloxone) and psychological (stress) activation of the hypothalamic-pituitary-adrenal (HPA) axis. Healthy subjects (mean age 25.2 years, SD 9.2 years) completed a naloxone challenge (n=74) and/or the modified Trier Social Stress Test (TSST) (n=86). For the naloxone challenge, two baseline blood samples were obtained. Then, five increasing doses of i.v. naloxone were administered at 30-min intervals and 12 additional blood samples were collected at 15-min intervals. The TSST consisted of 5-min of public speaking and 5-min of mental arithmetic exercises. Three baseline and five post-TSST blood samples were drawn. Both the naloxone and TSST groups had significant adrenocorticotropin (ACTH) and cortisol responses to their respective challenges (P<0.001). There were no differences in baseline ACTH, baseline cortisol, or ACTH response by genotype in either the naloxone or the TSST group. Among subjects expressing a G allele, there was a higher cortisol response to naloxone (P=0.046), but a lower cortisol response to the TSST (P=0.044). In conclusion, the minor allele (G) was associated with a robust cortisol response to naloxone blockade, but a blunted response to psychosocial stress. We speculate that increased opioid avidity of the minor allele receptor contributes to the differential response to naloxone vs stress.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenocorticotropic Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrocortisone,
http://linkedlifedata.com/resource/pubmed/chemical/Naloxone,
http://linkedlifedata.com/resource/pubmed/chemical/Narcotic Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0893-133X
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| pubmed:author | |
| pubmed:copyrightInfo |
Neuropsychopharmacology (2006) 31, 204-211. doi:10.1038/sj.npp.1300856; published online 3 August 2005.
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| pubmed:issnType |
Print
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| pubmed:volume |
31
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
204-11
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| pubmed:dateRevised |
2011-5-18
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| pubmed:meshHeading |
pubmed-meshheading:16123758-Adolescent,
pubmed-meshheading:16123758-Adrenocorticotropic Hormone,
pubmed-meshheading:16123758-Adult,
pubmed-meshheading:16123758-Alleles,
pubmed-meshheading:16123758-DNA,
pubmed-meshheading:16123758-Female,
pubmed-meshheading:16123758-Genotype,
pubmed-meshheading:16123758-Humans,
pubmed-meshheading:16123758-Hydrocortisone,
pubmed-meshheading:16123758-Male,
pubmed-meshheading:16123758-Naloxone,
pubmed-meshheading:16123758-Narcotic Antagonists,
pubmed-meshheading:16123758-Polymorphism, Single Nucleotide,
pubmed-meshheading:16123758-Receptors, Opioid, mu,
pubmed-meshheading:16123758-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16123758-Smoking,
pubmed-meshheading:16123758-Social Environment,
pubmed-meshheading:16123758-Stress, Psychological
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| pubmed:year |
2006
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| pubmed:articleTitle |
The mu-opioid receptor polymorphism A118G predicts cortisol responses to naloxone and stress.
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| pubmed:affiliation |
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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