AMPHETAMINE-INDUCED RELEASE OF DENDRITIC DOPAMINE IN SUBSTANTIA-NIGRAPARS RETICULATA - D1-MEDIATED BEHAVIORAL AND ELECTROPHYSIOLOGICAL EFFECTS

Dopamine (DA) released from dendrites of substantia nigra dopaminergic neurons potentially is in a position to modulate basal ganglia output s from the substantia nigra pars reticulata (SNR) via stimulation of D 1 receptors on the terminals of striatonigral afferents. The effects o f endogenous DA release in the SNR were examined in rats using behavio ral activation, multiunit activity of SNR neurons, and cortical EEG pa ttern as dependent measures. Unilateral infusion of amphetamine (AMPH) into SNR (10 mu g/0.5 mu l; 5 min) produced a short-lasting behaviora l activation that; was blocked by coinfusion of the D1 DA receptor ant agonist SCH 23390 (0.5 mu g). Multiunit recordings of SNR neurons in a nesthetized rats showed that AMPH, infused as above, produced a rapid decrease in SNR activity. This decrease was maximal (similar to 90%) d uring the first 10 min postinfusion, followed by a gradual return to b aseline levels. Coinfusion of SCH 23390 blocked the AMPH-induced decre ase in SNR activity, although by itself this drug produced a 40% decre ase in activity. Cortical EEG acquired during the SNR, infusions/recor dings showed a short-duration change in pattern immediately after AMPH infusion. A relative shift in power from the lowest frequency interva l determined (0.8-2.7 Hz) to the next higher frequency interval (2.7-6 .8 Hz) was observed which could be prevented by coinfusion of SCH 2339 0. Thus, dendritically released DA can inhibit the activity of SNR neu rons via local stimulation of D1 receptors. This effect is associated with a brief behavioral activation and EEG desynchronization. (C) 1996 Wiley-Liss, Inc.