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

Fig. 5.

Fig. 5.

Deletion of Grin1 exon 5 leads to an increase in the number of excitatory synapses in layer 5 pyramidal neurons in the cortex. (A, Left) A schematic view of the recording method. (A, Right) Normalized NMDAR-EPSCs recorded from WT and Grin1ΔEx5/ΔEx5 mice at P17-18. (B) Weighted decay constants of NMDAR-EPSCs from WT (22 cells from 4 mice) and Grin1ΔEx5/ΔEx5 neurons (24 cells from 4 mice) at P17-18. ****P < 0.0001, Mann–Whitney U test. (C) Examples of mEPSCs recorded layer 5 pyramidal neurons in a WT and a Grin1ΔEx5/ΔEx5 mouse at P18. (Scale bars, 100 ms, 20 pA.) (D and E) Frequency and amplitude of mEPSCs from WT (33 cells from 4 mice) and mutant neurons (30 cells from 4 mice) at P17-18. ****P < 0.0001; NS, P > 0.05, Mann–Whitney U test. The mean rise time of mEPSCs was 0.48 ± 0.02 ms for WT and 0.48 ± 0.01 ms for mutant (P = 0.43). The mean decay time of mEPSC was 2.53 ± 0.05 ms for WT and 2.55 ± 0.05 ms for mutant (P = 0.81). (F) Examples of dendritic spines along apical dendrites of layer 5 pyramidal neurons from WT and Grin1ΔEx5/ΔEx5 at P18. (Scale bar, 4 μm.) (G and H) Spine density of apical and basal dendrites of WT (18 cells from 4 mice) and Grin1ΔEx5/ΔEx5 neurons (16 cells from 4 mice) at P17-18. ***P < 0.001, Mann–Whitney U test.