Rixt van der Veen1, Pier Vincenzo Piazza, Véronique Deroche-Gamonet. 1. Centre de recherche INSERM U862 Physiopathologie de la plasticité neuronale, Institut François Magendie, Université de Bordeaux 2, 146 rue Léo Saignat, 33077 Bordeaux Cedex, France.
Abstract
RATIONALE: Individual differences in cocaine-taking behavior and liability to develop abuse are clearly observed, but underlying mechanisms are still poorly understood. A role for gene-environment interactions has been proposed but remains hypothetical. OBJECTIVES: We investigated whether gene-environment interactions influence intravenous cocaine self-administration (SA) in mice. We tested the effect of a past short group housing experience on cocaine SA in two inbred strains of mice, the C57BL/6J (C57) and DBA/2J (DBA). METHODS: Adult C57 and DBA mice were individually housed upon arrival in the laboratory. After 3 weeks, half of the animals of each strain were group housed for 19 days. One week after the end of group housing, cocaine SA or measurement of brain cocaine levels took place. RESULTS: Individually and ex-group-housed C57 mice did not differ for cocaine SA. On the contrary, the ex-group-housed DBA mice showed an upward shift in the dose-response curve as compared to individually housed DBA. Differences in brain cocaine levels could not account for the observed behavioral differences. CONCLUSIONS: These results demonstrate that vulnerability to cocaine reinforcing effects can be affected by gene-environment interactions. We propose a mouse model for the characterization of gene-environment interactions in the vulnerability to cocaine-taking behavior.
RATIONALE: Individual differences in cocaine-taking behavior and liability to develop abuse are clearly observed, but underlying mechanisms are still poorly understood. A role for gene-environment interactions has been proposed but remains hypothetical. OBJECTIVES: We investigated whether gene-environment interactions influence intravenous cocaine self-administration (SA) in mice. We tested the effect of a past short group housing experience on cocaine SA in two inbred strains of mice, the C57BL/6J (C57) and DBA/2J (DBA). METHODS: Adult C57 and DBA mice were individually housed upon arrival in the laboratory. After 3 weeks, half of the animals of each strain were group housed for 19 days. One week after the end of group housing, cocaine SA or measurement of brain cocaine levels took place. RESULTS: Individually and ex-group-housed C57 mice did not differ for cocaine SA. On the contrary, the ex-group-housed DBA mice showed an upward shift in the dose-response curve as compared to individually housed DBA. Differences in brain cocaine levels could not account for the observed behavioral differences. CONCLUSIONS: These results demonstrate that vulnerability to cocaine reinforcing effects can be affected by gene-environment interactions. We propose a mouse model for the characterization of gene-environment interactions in the vulnerability to cocaine-taking behavior.
Authors: Glenn A Doyle; X Rebecca Sheng; Candice L Schwebel; Thomas N Ferraro; Wade H Berrettini; Russell J Buono Journal: Neurosci Res Date: 2006-04-27 Impact factor: 3.304
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