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

Figure 3.

Figure 3

DAPK1 inhibition exerts rapid anti-seizure effects. Mice (C57BL/6, male, P56-P80, n = 12/group) were implanted with electrodes, allowed to recover for 7 days, and then pretreated with a DAPK1 inhibitor, vehicle or C6 (10 mg/kg) for 30 min followed 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 analysis, and the remaining animals continued to undergo behavioral analysis and EEG recording for 15 min. A-C C6 pretreatment decreases DAPK1 activity after PTZ. The brain lysates were subjected to immunoblotting analysis with anti-pSer308-DAPK1, anti-DAPK1, or anti-β-actin antibodies. Statistical significance was determined by one-way ANOVA with Tukey's multiple comparisons tests (***P < 0.001). D Representative EEG traces from saline or PTZ are shown for the vehicle- or DAPK1 inhibitor-treated group. E-G DAPK1 inhibitor-treated mice displayed lower seizure scores (E), longer latency to GTCS (F) and lower amplitude of GTCS (G) post PTZ administration. Statistical significance was determined by one-way ANOVA with Tukey's multiple comparisons test (E) or two-tailed Student's t tests (F and G) (**P < 0.01 and ***P < 0.001). n.s., no significance. All data shown represent the means ± standard errors of three independent experiments.