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. 2021 Jun 11;17(9):2356–2366. doi: 10.7150/ijbs.59922

Figure 2.

Figure 2

DAPK1 deletion exerts rapid anti-seizure effects in mice. Mice (C57BL/6, male, P56-P80, n = 12/group) were implanted with electrodes, allowed to recover for 7 days, and then insulted by a convulsive dose of PTZ (50 mg/kg). Brain tissues from a number of the animals (n = 4) were collected 3 min after PTZ administration for immunoblotting and immunoprecipitation analysis, and the remaining animals continued to undergo behavioral analysis and EEG recording for 15 min. A Representative EEG traces from saline or PTZ administration are shown for WT and DAPK1 KO mice. B-D DAPK1 deletion mice displayed lower seizure scores (B), longer latency to GTCS (C) and lower amplitude of GTCS post PTZ administration compared to WT littermates (D) (***P < 0.001 vs control, two-tailed Student's t-tests). E-G Enhanced interaction between NR2B and DAPK1 in the hippocampus after PTZ exposure (***P < 0.001 vs control, two-tailed Student's t tests). H-J Brain lysates were subjected to immunoblotting analysis with anti-pSer1303-NR2B, anti-NR2B, anti-pSer308-DAPK1, anti-DAPK1, anti-pSer19-MLC, anti-MLC or anti-β-actin antibodies. Statistical significance was determined by one-way ANOVA with Tukey's multiple comparisons tests (***P < 0.001). n.s., no significance. All data shown represent the means ± standard errors of three independent experiments.