Figure 9. Excitatory D1Rs and inhibitory A₁, D2 and CB₁Rs modulate presynaptic inputs in Drd2-EGFP mice.

A, the D1R agonist SKF38393 increased the frequency of mEPSCs by boosting the high-frequency, low-amplitude spontaneous inward currents but did not change the cumulative distribution of mEPSC amplitudes. For all panels, *P < 0.05, **P < 0.01, ***P < 0.001, Student's t test with Bonferroni adjustment and #P < 0.05, ##P < 0.01, Student's paired t test. B, adenosine reduced the frequency of mEPSCs by broadly decreasing high-frequency, low-amplitude currents and did not change the mEPSC amplitude distribution. C, the D2R agonist quinpirole reduced the frequency of mEPSCs by specifically reducing high-frequency, low-amplitude inward currents but did not change the cumulative amplitude distribution. D, the CB₁R agonist WIN55-2,2 decreased mEPSC over a wide range of frequencies and did not changes their amplitude distributions. E, amphetamine increased the frequency, but not the amplitude of sEPSCs in D2R+ cells. The D2R antagonist sulpiride blocked inhibition and the frequency of 5–10 pA inward currents increased. F and G, the frequency of sEPSCs was reduced by amphetamine with AM251 in D2+ cells (F), and also by amphetamine in MSNs from CB₁^−/− mice (G).