| pubmed-article:11590970 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11590970 | lifeskim:mentions | umls-concept:C0001973 | lld:lifeskim |
| pubmed-article:11590970 | lifeskim:mentions | umls-concept:C0001948 | lld:lifeskim |
| pubmed-article:11590970 | lifeskim:mentions | umls-concept:C0314657 | lld:lifeskim |
| pubmed-article:11590970 | lifeskim:mentions | umls-concept:C0205752 | lld:lifeskim |
| pubmed-article:11590970 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:11590970 | pubmed:dateCreated | 2001-10-9 | lld:pubmed |
| pubmed-article:11590970 | pubmed:abstractText | There is increasing evidence supporting a link between the endogenous opioid system and excessive alcohol consumption. Acute or light alcohol consumption stimulates the release of opioid peptides in brain regions that are associated with reward and reinforcement and that mediate, at least in part, the reinforcing effects of ethanol. However, chronic heavy alcohol consumption induces a central opioid deficiency, which may be perceived as opioid withdrawal and may promote alcohol consumption through the mechanisms of negative reinforcement. The role of genetic factors in alcohol dependency is well recognized, and there is evidence that the activity of the endogenous opioid system under basal conditions and in response to ethanol may play a role in determining an individual's predisposition to alcoholism. The effectiveness of opioid receptor antagonists in decreasing alcohol consumption in people with an alcohol dependency and in animal models lends further support to the view that the opioid system may regulate, either directly or through interactions with other neurotransmitters, alcohol consumption. A better understanding of the complex interactions between ethanol, the endogenous opioids and other neurotransmitter systems will help to delineate the neurochemical mechanisms leading to alcoholism and may lead to the development of novel treatments. | lld:pubmed |
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