Abstract

In vivo electrochemical recordings, coupled with local application of drugs from micropipettes, were used to determine the presynaptic effects of phencyclidine (PCP) on dopamine-containing nerve terminals in the intact rat striatum. Local application of PCP did not elicit an observable increase in extracellular levels of the monoamine neurotransmitters. However, pretreatment with PCP significantly potentiated the potassium-evoked release of monoamines. Nomifensine, a potent catecholamine reuptake blocker, produced effects that were analogous with PCP. Local pretreatment with PCP was also found to potentiate the electrochemical signal detected after pressure ejection of dopamine directly into the caudate nucleus. Finally, electrophysiological studies showed that locally applied PCP and nomifensine solutions had similar potencies in depressing the spontaneous firing of striatal neurons. Taken together, these data suggest that the major presynaptic action of PCP in the rat caudate nucleus is inhibition of the reuptake, and not alteration of release, of the monoamine neurotransmitters.