Skip to main content
. 2017 Oct 6;49(6):824–833. doi: 10.1111/ejn.13715

Figure 6.

Figure 6

NMDAR currents at PfN—but not cortical—synapses onto ChIs are potentiated by D5R activation. (A) Averaged optogenetic EPSC from PfN fibers in Vglut2‐Cre mice evoked in ChIs clamped at +40 mV (left) and ‐70 mV (right) before (black) and after (gray) application of SKF‐81297, a D1‐like receptor agonist. (B) Boxplots of the amplitude of the NMDA component (left, measured at +40 mV); the AMPA component (middle, 1st EPSC, measured at ‐70 mV); and the PPRs (right) demonstrate a significant amplification of the NMDA current without a concurrent change in the AMPA current or a change in the PPRs. (C) Averaged optogenetic EPSC from nominally cortical fibers in Thy1‐ChR2 mice evoked in ChIs clamped at +40 mV (left) and ‐70 mV (right) before (black) and after (gray) application of SKF‐81297. B. Boxplots of the amplitude of the NMDA component (left, measured at +40 mV); the AMPA component (middle, 1st EPSC, measured at −70 mV); and the PPRs (right) failed to demonstrate any change in the NMDA or AMPA currents or a change in the PPRs.