Figure 8.

Time course of action of dopaminergic drugs. IPSCs exhibited amplitude variation from trial to trial, suggesting that only a few terminals were being activated. Amplitudes in each trial and mean amplitude of first IPSC were graphed in all cases (A-D). A, IPSCs were evoked with antidromic stimulation from the GP, thus favoring activation of terminals from recurrent axon collaterals (as in Fig. 1C). After several minutes of control recordings, 200 nm quinelorane (dopaminergic D₂ receptor agonist) was added to the superfusion. Quinelorane reduced IPSC amplitude and produced paired-pulse facilitation (PPR >1). Recordings at right, in this and the other frames, were taken before and during drug application, as indicated by the numbers. B, Same experimental arrangement as in A, except that 200 nm SKF 81297 (dopaminergic D₁ receptor agonist) was administered. A tendency to exhibit larger IPSC amplitudes is accompanied with paired-pulse depression (PPR <1). C, IPSCs are now intrastriatally evoked (as in Fig. 1 B). Quinelorane produced neither amplitude nor PPR changes in most cases. D, Same experimental arrangement as in C, except that SKF 81297 is administered. In this case, there was no consistent change of either mean amplitude or PPR. In several cases, the IPSC was reduced. Stimulus frequency was 0.2 Hz. The traces at right are averages of 2 min recordings at approximate times indicated by the numbers.