Differential propensity to ethanol sensitization is not associated with altered binding to D1 receptors or dopamine transporters in mouse brain.

Behavioral sensitization to ethanol's stimulant effect has been proposed as a marker for individual abuse liability. In previous work we have demonstrated that mice showing an increased propensity to EtOH sensitization had higher levels of dopamine (DA) D2 receptor binding in localized brain areas compared to mice showing less sensitization. In the present study we examined whether altered binding to D1 or the DA transporter (DAT) might also be associated with differential propensity to develop EtOH sensitization. Male Swiss mice received 2.4 g/kg EtOH or saline intraperitoneally (i.p.) daily for 21 days, were tested weekly for locomotor activity, and then sacrificed. D1 and DAT binding were assessed by quantitative autoradiography using [(3)H]SCH-23390 and [(3)H]WIN 35,428, respectively. EtOH-treated mice were subdivided into sensitized and non-sensitized subgroups according to their locomotor activity during treatment. Analyses of brain D1 (19 regions) and DAT (12 regions) binding densities revealed no significant differences among EtOH-sensitized, -non-sensitized or saline groups in any of the regions measured (all p values > 0.32 for D1 and > 0.16 for DAT). These results suggest that brain D1 and DAT binding, unlike the recently reported changes in D2 binding, do not differentiate mice that develop behavioral sensitization to ethanol from those that do not.