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Ethanol-induced behavioral sensitization is associated with dopamine receptor changes in the mouse olfactory tubercle

pmid: 18761028
Accumulating evidence points to the mesolimbic and the nigrostriatal dopamine systems as critical to behavioral sensitization induced by several drugs of abuse. In the present study, we analyzed D1 and D2 binding to brain regions related to these dopaminergic systems during the expression of ethanol-induced behavioral sensitization. The first experiment was performed to demonstrate the effectiveness of the ethanol treatment schedule and challenge used to induce the expression of the behavioral sensitization phenomenon. The second experiment was conducted to study D1 and D2 alterations in several brain regions during the expression of this phenomenon. Mice were ip treated with ethanol or saline for 21 consecutive days and 24 h after the last injection they received an ethanol or a saline challenge injection. Five minutes later, the animals were observed in an open-field for locomotion quantification or were sacrificed and their brains were submitted to autoradiographic binding analyses. No differences among the groups were found for D1 binding levels in all the brain regions analyzed. However, ethanol-sensitized mice showed reduced levels of D2 binding in the olfactory tubercle when compared to the other groups. Our data suggest that D2 receptor changes in the olfactory tubercle seem to play an important role in the expression of ethanol-induced behavioral sensitization.
- Federal University of São Paulo Brazil
- Universidade de São Paulo Brazil
Analysis of Variance, Behavior, Animal, Ethanol, Brain, Central Nervous System Depressants, Olfactory Pathways, Benzazepines, Receptors, Dopamine, Mice, Raclopride, Animals, Autoradiography, Dopamine Antagonists, Female, Locomotion, Protein Binding
Analysis of Variance, Behavior, Animal, Ethanol, Brain, Central Nervous System Depressants, Olfactory Pathways, Benzazepines, Receptors, Dopamine, Mice, Raclopride, Animals, Autoradiography, Dopamine Antagonists, Female, Locomotion, Protein Binding
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