Extracellular single unit recordings were used to determine the effects of systemically and iontophoretically applied phencyclidine on electrophysiologically-identified A10 dopamine neurons within the ventral tegmental area of the rat. Intravenous injections of phencyclidine inhibited, as well as excited A10 cells. Approximately 42% of the inhibitions induced by phencyclidine were completely reversed by an injection of haloperidol. The excitatory effects of phencyclidine most often resulted in a state of depolarized inactivation and were not sensitive to haloperidol. The alteration of the activity of A10 cells by systemically-applied phencyclidine was effectively prevented in all animals pretreated with a combination of reserpine and alpha-methyl-p-tyrosine, which depleted stores of central catecholamines by over 90%. In contrast to the data obtained with intravenous injections, iontophoretic applications of phencyclidine produced only inhibition of the activity of the A10 cells and, in a few of these cases the decreased firing rate was accompanied by an increase in the amplitude of the action potential. A comparison of the response patterns of dopaminergic neurons to systemically- and iontophoretically-applied phencyclidine would suggest that excitations induced by phencyclidine are not mediated at the level of the A10 cell bodies but through a site outside the ventral tegmental area. The results of this study also indicate that some of the effects of phencyclidine on the activity of A10 neurons are clearly dependent upon an interaction with dopamine and thus, would support the hypothesis that phencyclidine can act as an indirect dopamine agonist. However, other effects of phencyclidine which are not apparently linked to dopamine may represent the response of a pharmacologically-distinct subpopulation of A10 neurons to phencyclidine.