Abstract
Concurrent use of cocaine and alcohol results in reinforced behavioral consequences, but the molecular mechanisms associated with the co-use of both drugs are not clear. We report here that a 24-h exposure of the human dopamine transporter (hDAT)-transfected mouse neuroblastoma N1E-115 cell line (6C6) to cocaine (1 μM), or ethanol (1%) or both, increased dopamine re-uptake by approximately 25, 29 and 44%, respectively. The same treatment also increased dopamine re-uptake by the hDAT-transfected mouse neuroblastoma Neuro2A cell line (3B7) by approximately 36, 41 and 77%, respectively. However, no increase of dopamine re-uptake was observed in the hDAT-transfected non-neuronal CHO cell line (10E9). These data support the hypothesis that the DAT may be a common neural substrate for cocaine and ethanol in dopaminergic neurons and it may be involved in the psychological effects of both addictions.
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