Figure 2.

Ifenprodil, a GluN2B antagonist, reduces NMDAR-mediated EPSCs by the same relative degree in saline and cocaine groups. A, B, Within-cell application of ifenprodil (5 μm) to saline cells (5 cells/4 rats) significantly reduced response amplitudes at 40 mV (saline vs saline +ifenprodil, paired t test, t₍₄₎ = 2.88, p = 0.045), but not –80 mV (saline vs saline +ifenprodil, paired t test, t₍₄₎ = 0.052, p = 0.9613). These data suggest that GluN2B-containing NMDARs are present under control conditions but only contribute at depolarized membrane potentials. C, D, In cocaine WD5 cells (5 cells/3 rats), within-cell application of ifenprodil significantly reversed the increased amplitudes at 40 mV (cocaine WD5 vs cocaine WD5 +ifenprodil, paired t test, t₍₄₎ = 7.101, p = 0.0021). A trend was observed at –80 mV (cocaine WD5 vs cocaine WD5 +ifenprodil, paired t test, t₍₄₎ = 1.921, p = 0.12). E, F, In cocaine WD > 39 cells, within-cell application of ifenprodil (6 cells/5 rats) reversed the cocaine-induced increases in response amplitudes at both negative and positive holding potentials. 40 mV: cocaine WD > 39 versus cocaine WD > 39 +ifenprodil, paired t test, t₍₅₎ = 4.578, p = 0.006; –80 mV: cocaine WD > 39 versus cocaine WD > 39 +ifenprodil, paired t test, t₍₅₎ = 3.46, p = 0.018. G, Representative traces. Calibration: 40 mV, 50 pA × 250 ms; –80 mV, 20 pA × 250 ms. *p < 0.05.