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. 2016 Jun 22;36(25):6778–6791. doi: 10.1523/JNEUROSCI.4092-15.2016

Figure 5.

Figure 5.

GluN2B-mediated NMDAR-EPSCs are increased in arg−/− hippocampal slices. A, Loss of Arg increases GluN2B-containing NMDAR-EPSC amplitude. Ai, Left, Representative traces of NMDAR-EPSCs recorded from CA1 hippocampal neurons with or without the GluN2B antagonist Ifenprodil (Ifen) from WT and arg−/− hippocampal slices at P42. Ai–Aiii, Loss of Arg increases NMDAR-EPSCs compared with WT. Ifenprodil partially blocks both WT and arg−/− NMDAR-EPSCs at P21 (Ai), P31 (Aii), and P42 (Aiii). Note that ifenprodil treatment blocks the increased NMDAR-EPSCs in arg−/− neurons to levels comparable to those of WT + Ifen. *p < 0.05, **p < 0.01 vs WT; ##p < 0.01 vs arg−/−. B, Ifenprodil blocks a larger portion of the NMDAR-EPSC in arg−/− neurons. Histogram represents the percentage of the NMDAR-EPSC that is sensitive and insensitive to ifenprodil. C, Block of GluN2B-containing NMDARs silences high-Pr synapses in arg−/− neurons. Five minutes of ifenprodil treatment reduces NMDAR-EPSC amplitude in CA1 neurons from arg−/− slices faster than in WT neurons. The addition of MK801 after 5 min further inhibits NMDAR-EPSCs, but at a similar rate in WT and arg−/−. Inset, When NMDAR-EPSC amplitudes are renormalized to the time of MK801 addition, it is evident that the rate of MK801 inhibition of NMDAR-EPSC amplitude in WT (gray circles) and arg−/− (black circles) neurons is not different. The stimulus interval is 20 s.