Baclofen reduces ethanol intake in high-alcohol-drinking University of Chile bibulous rats

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Abstract:

ABSTRACT

Treatment with γ-aminobutiric acid (GABAB) receptor agonist, ±baclofen, has been shown to reduce ethanol intake in selectively bred Sardinian alcohol-preferring rats. The general goal of the present study was to characterize the high ethanol consumption high-alcohol-drinking University of Chile bibulous (UChB) rats with regard to the anti-alcohol effect of GABAB receptor stimulation. UChB rats were treated with the more active enantiomer of baclofen [R(+)-baclofen; at a dose of 1.0, 2.0 or 3.0 mg/kg] administered intraperitoneally once daily for four consecutive days or a single dose. When comparing ethanol and saccharin consumption in a free-choice regimen with unlimited access 24 hours/day, the dose of baclofen required to attenuate ethanol consumption significantly was 1.0 mg/kg administered once a day for three consecutive days while the dose that was sufficient to affect saccharin consumption significantly was 2.0 mg/kg, indicating that baclofen was more potent in reducing ethanol intake by UChB rats than reducing saccharin consumption. The reduction of ethanol or saccharin intake can not be attributed to baclofen-induced motor impairment, since baclofen (1.0, 2.0 or 3.0 mg/kg) did not alter spontaneous locomotor activity in UChB rats. Baclofen dose-dependently suppressed the motor activity stimulated by ethanol administration, a phenomenon mediated by activation of the mesolimbic dopamine system. In conclusion, these results showed that the activation of GABAB receptor by R(+)-baclofen reduced ethanol and saccharin consumption, as well as ethanol-induced motor stimulation, implicating the GABAB receptor in the neural substrates mediating effects that sustain voluntary ethanol in take in UChB rats.

Keywords: Baclofen; GABAB; UChB rats; ethanol intake; locomotor activity; saccharin intake

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1369-1600.2008.00102.x

Publication date: September 1, 2008

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