The preceding data suggest that the primary effect of repeated AD administration on most midbrain DA neurons is inactivation. This depolarization-induced cessation of spontaneous activity would appear to have a marked effect on both basal and stimulated DA release from nerve terminals in that several studies, using voltametric techniques, have now demonstrated DA release to be diminished under these conditions. These findings stand in marked contrast to the acute effects of ADs where biochemical techniques have been used to demonstrate a marked increase in the release of DA into projection areas. The combined effects of acute and repeated AD administration on midbrain DA cell activity may explain the delay in onset of both their therapeutic and neurological side effects.