Cocaine binding sites in mouse striatum, dopamine autoreceptors, and cocaine-induced locomotion

BALB/cByJ mice received cocaine (25 mg/kg IP) once a day for 3 days, resulting in a greater locomotor response to cocaine on day 3 than on day 1. On day 4, a dose (0.03 mg/kg SC) of apomorphine, targeted at dopamine autoreceptors, caused the same degree of locomotor depression in cocaine- as in saline-pretreated mice. In addition, no change was found in either the affinity or density of cocaine binding sites in their striatum as measured by the binding of [3H]CFT. C57BL/6ByJ, mice displayed a greater locomotor response to cocaine than BALB/cByJ mice, but had the same number of striatal [3H]CFT binding sites with the same affinity. Factors other than striatal cocaine binding sites, or dopamine autoreceptors as measured by apomorphine-induced depression of locomotion, should be considered for the explanation of the enhancement of the locomotor response upon daily cocaine administration in BALB/cByJ mice, or for the different locomotor response to cocaine of this strain compared with the C57BL/6ByJ strain of mice.