Fig. 10.

A low concentration of R-CPP did not inhibit somato-dendritic NMDA receptor currents in stellate cells. A and B: outside-out somatic patches were excised from stellate cells from WT mice (A), and NMDA receptor currents were recorded during the application of 10 μM NMDA and 10 μM glycine (B). After establishment of a stable baseline, R-CPP (0.2 μM) that blocks tri-GluN2B/2D was added to the superfusion medium. B: group data showing that R-CPP had no effect, suggesting that tri-GluN2B/2D NMDA receptors are not expressed in the somata of stellate cells. C: dendritic NMDA receptor currents were evoked by a train of PF stimulation at 100 Hz (4 stimuli). Currents were recorded at +40 mV in stellate cells before (black traces) and during (gray traces) superfusion of an NMDA receptor blocker. R-CPP (0.2 μM) did not reduce the PF-evoked NMDA receptor current. D–F: R-CPP (0.2 μM) did not alter the amplitude (D), charge transfer (E), and decay time (F) of dendritic NMDA receptor currents (open circles indicate data from individual experiments). In WT mice, NMDARs that are sensitive to a low concentration of R-CPP, including tri-GluN2B/2D receptors, are not present on the soma of stellate cells. R-CPP prevented I-LTP but did not inhibit dendritic currents; therefore, I-LTP, which requires tri-GluN2B/2D receptors (Figs. 5 and 6), is not triggered by a somato-dendritic depolarization.