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Glycyl-glutamine in nucleus accumbens reduces ethanol intake in alcohol preferring (P) rats.
- Source :
-
Brain research [Brain Res] 2005 Oct 05; Vol. 1058 (1-2), pp. 73-81. Date of Electronic Publication: 2005 Oct 05. - Publication Year :
- 2005
-
Abstract
- Opioid peptides and glycyl-glutamine (Gly-Gln) have been implicated in the control of ethanol consumption. A recognized beta-endorphin cleavage product, Gly-Gln, inhibits voluntary alcohol consumption when microinjected into the nucleus accumbens (AcbSh) of P rats. To evaluate the site-specific efficacy of Gly-Gln on ethanol consumption following AcbSh application, ethanol preferring (P) rats were allowed to establish individual baseline ethanol/water consumption utilizing a voluntary self-administration paradigm. Subsequent to baseline ethanol consumption being established, bilateral guide cannulae were stereotaxically implanted +1 mm dorsal to the AcbSh for subsequent Gly-Gln (100 nmol/microl) or saline vehicle (1 microl) injections. Alcohol intake, body weight, and water intake were measured at 24 h post-injection intervals. Unilateral Gly-Gln injections reduced ethanol consumption 35.6% (P < 0.05) from pre-established baseline consumption (6.24 +/- 0.64 g/kg to 4.06 +/- 0.28 g/kg). Bilateral Gly-Gln injections further reduced consumption to 51.9% (6.4 +/- 1.0 g/kg to 3.08 +/- 0.65 g/kg at 24 h (P < 0.01) below established baseline values within 24 h without significant changes in body weight or water consumption. Also, the amino acid constituents of the dipeptide had no influence on ethanol consumption behavior; however, Gly-Gln efficacy was shown to be comparable to central beta-endorphin-(1-27) or intraperitoneal (i.p.) naltrexone-induced suppression of ethanol intake. These data indicate that the AcbSh exhibits a site-specific sensitivity to the suppressive actions of Gly-Gln or beta-endorphin-(1-27) injections that modulate voluntary ethanol consumption in P rats. These findings support the broader concept that select forebrain opioid-responsive neural sites may influence the development or expression of alcohol abuse syndromes in animal models or humans.
- Subjects :
- Alcohol-Induced Disorders, Nervous System metabolism
Alcohol-Induced Disorders, Nervous System physiopathology
Alcoholism drug therapy
Animals
Central Nervous System Depressants adverse effects
Disease Models, Animal
Genetic Predisposition to Disease genetics
Narcotic Antagonists pharmacology
Nucleus Accumbens metabolism
Nucleus Accumbens physiopathology
Rats
Rats, Mutant Strains
Receptors, Opioid agonists
Receptors, Opioid metabolism
beta-Endorphin analogs & derivatives
beta-Endorphin metabolism
beta-Endorphin pharmacology
Alcohol-Induced Disorders, Nervous System drug therapy
Dipeptides pharmacology
Ethanol adverse effects
Nucleus Accumbens drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1872-6240
- Volume :
- 1058
- Issue :
- 1-2
- Database :
- MEDLINE
- Journal :
- Brain research
- Publication Type :
- Academic Journal
- Accession number :
- 16212948
- Full Text :
- https://doi.org/10.1016/j.brainres.2005.07.066