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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Neuropharmacology. 2016 Oct 23;113(Pt A):386–395. doi: 10.1016/j.neuropharm.2016.10.021

Figure 2. Src selectively enhances GluN2B-NMDAR EPSCs in CA1 pyramidal cells of naive rats.

Figure 2

Pharmacologically isolated GluN2B-NMDAR EPSCs (A, C) and GluN2A-NMDAR EPSCs (B, D) were recorded in CA1 pyramidal cells of naive rats using the GluN2A-selective antagonist NVP-AAM077 (NVP; 50 nM) and the GluN2B-selective antagonist ifenprodil (Ifen; 3 µM), respectively. Time course of the effect of intracellular application of Src (A, B) or pYEEI + Src (40–58) peptide (C, D) through a patch pipette on GluN2B-NMDAR EPSCs (A, C) or GluN2A-NMDAR EPSCs (B, D) is shown as a percent change in amplitude (mean ± SEM). Amplitudes of GluN2B-NMDAR EPSCs (A, C) or GluN2A-NMDAR EPSCs (B, D) during the first 5–10 min and the period from 30 to 35 min were used to calculate a percent change for statistical analysis. Src enhances GluN2B-NMDAR EPSCs (A), but not GluN2A-NMDAR EPSCs (B). Co-application of pYEEI with Src (40–58) has no effect on both GluN2B-NMDAR EPSCs (C) and GluN2A-NMDAR EPSCs (D). **p < 0.01