Single unit recording techniques were used to determine the effects of intravenously and microiontophoretically administered phencyclidine (PCP) and the enantiomers of N-allylnormetazocine (SKF-10,047) on the activity of midbrain dopamine (DA) neurons. Intravenous PCP produced a biphasic effect on substantia nigra zona compacta (A9) and ventral tegmental (A10) DA neurons which consisted of excitation followed by inhibition below baseline firing rates as the dose was increased. The high-dose attenuation of firing by PCP, but not the excitatory effects, was antagonized by haloperidol pretreatment. Intravenous (+)- and (-)-SKF-10,047 increased the firing rate of most A9 and A10 DA neurons. In contrast to the intravenous findings, iontophoretic PCP generally exerted only very weak inhibitory actions on neuronal activity, while (+)- and (-)-SKF-10,047 produced no consistent effects. The results suggest that these drugs indirectly influence the activity of DA neurons and that this may be a property shared by drugs classified as sigma receptor agonists.