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. 2019 Sep 30;116(42):21207–21212. doi: 10.1073/pnas.1905721116

Fig. 4.

Fig. 4.

Distinct roles of GluN2A and exon-5-containing GluN1 in developmental remodeling of NMDARs at thalamic relay synapses. (A) Normalized NMDAR-EPSCs recorded at VPm relay synapses from Grin1ΔEx5/Grin2a DKO mice at P7, P11, and P16. Each trace is the averaged responses from 13 to 22 cells. (B) Weighted decay constants (τw) of NMDAR-EPSCs of the 4 groups from P7 to P16. Data for Grin1ΔEx5/Grin2a DKO were from 13 to 22 cells from 3 to 4 mice for each time point. Data for Grin2a-KO and WT were the same as in Fig. 1C and data for Grin1ΔEx5 were the same as in Fig. 2D. (C) A model of developmental remodeling of NMDARs implicating both N-terminal splicing of Grin1 and up-regulation of Grin2a.