Fig. 4.

Long-term nicotine and/or haloperidol treatment alters the striatal dopamine transporter, as well as α6β2* and α4β2* nAChR levels. Rats were chronically administered nicotine (2 mg/kg per day) and/or haloperidol (1 mg/kg) as described under Materials and Methods. After treatment, they were killed 90 min after the last injection of haloperidol. Top panel shows striatal dopamine transporter levels measured using [¹²⁵I]RTI-121. Long-term nicotine and haloperidol treatments resulted in a significant reduction in transporter levels, with no further reduction with the combined treatment. The middle panel depicts striatal α6β2* nAChR levels assessed using [¹²⁵I]α-CtxMII. Both nicotine and haloperidol treatments resulted in significant reductions in α6β2* nAChR levels, with no further decrease with the combined treatment. Striatal α4β2* nAChR levels were determined by measuring binding of [¹²⁵I]epibatidine in the presence of α-CtxMII. Nicotine treatment increased α4β2* nAChRs in the absence or presence of haloperidol, whereas long-term treatment of haloperidol alone led to a significant decrease in binding. Values are the mean ± S.E.M. of six rats in the vehicle and nicotine-treated and 12 rats in the haloperidol and nicotine + haloperidol-treated groups. Significance of difference from vehicle-treated control, ##, P < 0.01, ###, P < 0.001; from own vehicle-treated group, **, P < 0.01, ***, P < 0.001 using two-way ANOVA followed by a Bonferroni test.