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. Author manuscript; available in PMC: 2023 Jun 17.
Published in final edited form as: Sci Transl Med. 2022 Oct 5;14(665):eabn2956. doi: 10.1126/scitranslmed.abn2956

Fig. 8. Metabolic and pharmacologic treatment of G1D seizures.

Fig. 8.

(A) Dose-response relationship for induction of GTCS after pilocarpine administration. (B) Pretreatment of G1D mice with BKP effect on seizure threshold to pilocarpine-induced GTCS. (C) Dose-response relationship for the ability of diazepam to terminate early (blue) SE and late (black) GTCS in control mice (n = 6 to 8 mice per dose). The dose-response curve was obtained by plotting the percentage of mice that stopped seizing within 1 hour of treatment against the log dose of diazepam. ED50 values were obtained for early and late SE treatment groups. (D) Diazepam ability to terminate GTCS in control (blue) and G1D (red) mice. (E) Diazepam effect on GTCS termination when administered after 30 min of GTCS onset. (F) Representative EEG traces obtained at various times during a 24-hour period test the efficacy of diazepam administered immediately after the onset of pilocarpine-induced GTCS. (G) Dose-response for phenobarbital termination of GTCS in control animals. (H). Effect of phenobarbital on GTCS termination (I). Effect of the AMPA-kainate receptor antagonist GYKI-52466 on G1D mice with GTCS induced by pilocarpine, both early and late. *P < 0.05 compared to control (D, H, and I) or G1D (B).