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http://purl.uniprot.org/citations/17336938http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17336938http://www.w3.org/2000/01/rdf-schema#comment"

Background

Ethanol stimulates the dopaminergic mesoaccumbal pathway, which is thought to play a role in ethanol reinforcement. Mu (mu)-opioid (MOP) receptors modulate accumbal dopamine activity, but it is not clear whether MOP receptors are involved in the mechanism of ethanol-stimulated accumbal dopamine release.

Methods

We investigated the role that MOP receptors play in ethanol (2.0 g/kg)-stimulated accumbal dopamine release by using MOP receptor knockout mice (C57BL/6J-129SvEv and congenic C57BL/6J genotypes) along with blockade of MOP receptors with a mu1 selective antagonist (naloxonazine).

Results

Both gene deletion and pharmacological antagonism of the MOP receptor decreased ethanol-stimulated accumbal dopamine release compared with controls with female mice showing a larger effect in the C57BL/6J-129SvEv genotype. However, both male and female mice showed reduced ethanol-stimulated dopamine release in the congenic MOP receptor knockout mice (C57BL/6J). No differences in the time course of dialysate ethanol concentration were found in any of the experiments.

Conclusions

The data demonstrate the existence of a novel interaction between genotype and sex in the regulation of ethanol-stimulated mesolimbic dopamine release by the MOP receptor. This implies that a more complete understanding of the epistatic influences on the MOP receptor and mesolimbic dopamine function may provide more effective pharmacotherapeutic interventions in the treatment of alcoholism."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.org/dc/terms/identifier"doi:10.1016/j.biopsych.2006.11.016"xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Tang A."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Gonzales R.A."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Uhl G.R."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Bergeson S.E."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Sora I."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Hall F.S."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/author"Job M.O."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/name"Biol Psychiatry"xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/pages"627-634"xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/title"Mu (mu) opioid receptor regulation of ethanol-induced dopamine response in the ventral striatum: evidence of genotype specific sexual dimorphic epistasis."xsd:string
http://purl.uniprot.org/citations/17336938http://purl.uniprot.org/core/volume"62"xsd:string
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