Dopaminergic substrates of cocaine-induced place conditioning

Abstract

Recently, Spyraki et al. ( Brain Research, 253 (1982) 195–203) reported that cocaine-induced place preference conditioning was unaffected by blockade of central dopamine (DA) or norepinephrine function. In addition, systemic injections of the local anesthetic procaine produced place preference conditioning. The present study was undertaken to further evaluate the possible role of DA in coccaine-induced place conditioning. In Expt. 1, a partial replication of Spyraki et al., systemic cocaine (5.0 mg/kg, i.p.) produced significicant place conditioning that was not disrupted with the DA antagonist pimozide (1.0 mg/kg, i.p.). In Expt. 2, cocaine was microinjected unilaterally into the lateral ventricles to eliminate peripheral local anesthesia. Cocaine (50.0 μg, i.c.v.) produced place conditioning and pretreatment with pimozide (1.0 mg/kg, i.p.) disrupted the effect. In Expt. 3, place conditioning was not observed when cocaine presentations (50.0 μg, i.c.v.) were paired with both compartments. The substrates of cocaine-induced place conditioning were further investigated in Expt 4: Procaine (250 μg, i.c.v.) did not produce place conditioning whereas the DA agonist bromocriptine (50.0 μg, i.c.v.) did. Results suggest the involvement of central DA in cocaine-induced place conditioning.