Attenuation of the locomotor-sensitizing effects of the D2 dopamine agonist bromocriptine by either the D1 antagonist SCH 23390 or the D2 antagonist raclopride.

Abstract

Injections of the selective D2 dopamine agonist bromocriptine (5.0 mg/kg, IP) produced progressively stronger locomotion over 10 days of repeated testing. Concurrent treatment with either the D1 antagonist SCH 23390 (0.01 or 0.1 mg/kg, IP) or the D2 antagonist raclopride (0.1 or 1.0 mg/kg, IP) suppressed bromocriptine-induced locomotion on treatment days and attenuated or blocked the progressive increases in locomotion that accompanied repeated injections of bromocriptine alone. The fact that D1 and D2 antagonists each block the acute actions of bromocriptine and attenuate the development of bromocriptine sensitization is suggested to imply a striatal rather than a ventral tegmental mechanism for the sensitization produced by repeated treatments with direct dopamine agonists.