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| Research article summary (published 30 Jan 2009): |
Excessive alcohol consumption is blocked by glial cell line-derived neurotrophic factor.
Full Abstract
We previously found that activation of the glial cell line-derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) reduces moderate alcohol (ethanol) intake in a rat operant self-administration paradigm. Here, we set out to assess the effect of GDNF in the VTA on excessive voluntary consumption of ethanol. Long-Evans rats were trained to drink large quantities of a 20% ethanol solution in an intermittent-access two-bottle choice drinking paradigm. The rats were given three 24-h sessions per week, and GDNF's actions were measured when rats achieved a baseline of ethanol consumption of 5.5g/kg/24h. We found that microinjection of GDNF into the VTA 10min before the beginning of an ethanol-drinking session significantly reduced ethanol intake and preference, but did not affect total fluid intake. We further show that GDNF greatly decreased both the first bout of excessive ethanol intake at the beginning of the session, and the later consummatory activity occurring during the dark cycle. These data suggest that GDNF is a rapid and long-lasting inhibitor of "binge-like" ethanol consumption.
Author information
Author/s: Carnicella, Sebastien (S); Amamoto, Ryoji (R); Ron, Dorit (D);
Affiliation: The Ernest Gallo Research Center, 5858 Horton St, Ste 200, Emeryville, CA 94608, USA.
Grants: R01 AA014366-02 (Agency:NIAAA NIH HHS)
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Journal: Alcohol (Fayetteville, N.Y.) (Alcohol), published in United States. (Language: eng)
Reference: 2009-Feb; vol 43 (issue 1) : pp 35-43
Dates: Created 2009/02/02; Completed 2009/04/10;
PMID: 19185208, status: MEDLINE (last retrieval date: 4/10/2009, IMS Date: 10 Apr 2009 00:00:00)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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