Figure 3.

The “rebound” firing of CINs is not due to intrinsic membrane properties. A–C, Current-clamp traces from CINs in dorsal striatum upon somatic injection of hyperpolarizing current steps. A, Injection of small current steps (−30 pA, 200 ms) mimicking the amplitude and duration of the second outward current evoked by SNc neuron stimulation did not evoke an obvious rebound burst. B, Injection of larger current steps (−300 pA, 200 ms) evoked a prominent current sag potential (arrow) and rebound burst during and after the step, respectively, both of which were blocked by the HCN channel blocker ZD7288 (50 μm; C). D, E, Population perievent spike histograms of average spike discharge (solid lines) upon somatic injection of −30 pA (D; n = 8 cells) or −300 pA (E; n = 9 cells). Outlines depict SEM. For recordings in the presence of ZD2788 (50 μm), a small depolarizing current (50–80 pA) was continuously applied to the recording pipette to sustain firing. F, Example voltage response of a CIN upon optogenetic stimulation of nigrostriatal afferents. Negative current was injected to prevent the cell from firing, thus revealing subthreshold membrane potential fluctuations. Light stimulation (blue arrow) evokes an initial hyperpolarization and a prominent delayed depolarization, indicating that modulation of CIN discharge by SNc neurons results from synaptically evoked fluctuations in somatic membrane potential.