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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-7-21
pubmed:abstractText
Evidence recently provided has suggested a specific involvement of the GABAergic system in modulating positive reinforcing properties of several drugs of abuse through an action on mesolimbic dopaminergic neurons. The GABA(B) receptor agonist baclofen has been proposed as a potential therapeutic agent for the clinical treatment of several forms of drug addiction. In the present study, using the in vivo microdialysis technique, we investigated the effect of baclofen on nicotine, cocaine, and morphine-induced increase in extracellular dopamine (DA) levels in the shell of the nucleus accumbens, a brain area supposedly involved in the modulation of the central effects of several drugs of abuse, of freely moving rats. As expected, nicotine (0.6 mg/kg s.c.), morphine (5 mg/kg s.c.), and cocaine (7.5 mg/kg i.p.) administration in rats induced a marked increase in extracellular DA concentrations in the nucleus accumbens, reaching a maximum value of +205 +/- 8.4%, +300 +/- 22.2%, and +370 +/- 30.7%, respectively. Pretreatment with baclofen (1.25 and 2.5 mg/kg i.p.) dose-dependently reduced the nicotine-, morphine-, and cocaine-evoked DA release in the shell of the nucleus accumbens. Furthermore, baclofen alone did not elicit changes in basal DA extracellular levels up to 180 min. Taken together, our data are in line with previous reports demonstrating the ability of baclofen to modulate the mesolimbic DAergic transmission and indicate baclofen as a putative candidate in the pharmacotherapy of polydrug abuse.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0887-4476
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-6
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12872287-Animals, pubmed-meshheading:12872287-Baclofen, pubmed-meshheading:12872287-Cocaine, pubmed-meshheading:12872287-Dopamine, pubmed-meshheading:12872287-Dose-Response Relationship, Drug, pubmed-meshheading:12872287-Extracellular Fluid, pubmed-meshheading:12872287-GABA Agonists, pubmed-meshheading:12872287-GABA-B Receptor Agonists, pubmed-meshheading:12872287-Male, pubmed-meshheading:12872287-Microdialysis, pubmed-meshheading:12872287-Morphine, pubmed-meshheading:12872287-Neural Pathways, pubmed-meshheading:12872287-Nicotine, pubmed-meshheading:12872287-Nucleus Accumbens, pubmed-meshheading:12872287-Rats, pubmed-meshheading:12872287-Receptors, GABA-B, pubmed-meshheading:12872287-Reward, pubmed-meshheading:12872287-Substance-Related Disorders, pubmed-meshheading:12872287-Synaptic Transmission, pubmed-meshheading:12872287-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
Baclofen antagonizes nicotine-, cocaine-, and morphine-induced dopamine release in the nucleus accumbens of rat.
pubmed:affiliation
B.B.Brodie Department of Neuroscience, University of Cagliari, 09042 Monserrato, Cagliari, Italy. pfadda@unica.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't