Effects of haloperidol (10(-7)-alpha 10(-5) M), trifluoperazine, metoclopramide, tiapride, sulpiride, thioridazine, clozapine remoxipride, raclopride, cis- and trans-isomers of carbidine, SCH 23390 (all at the 10(-6) M) on the K(+)-stimulated (28 mM) dopamine (DA) release from isolated rat striatum were studied. Haloperidol at the concentration of 10(-7) and 10(-6) M failed to affect, while at 10(-5) M the drug decreased the stimulated striatal DA release. Trifluoperazine, metoclopramide and tiapride were shown not to modify this process. Sulpiride, thioridazine, clozapine, remoxipride, raclopride, isomers of carbidine were found to increase significantly the stimulated striatal DA release. SCH 23390 failed to affect K(+)-stimulated release of DA in the striatum and also did not change K(+)-stimulated release enhancement produced by raclopride. It is suggested that the mechanism underlying observed effects of the drugs may contribute to pharmacological profile of atypical neuroleptics.