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. Author manuscript; available in PMC: 2013 Nov 15.
Published in final edited form as: Toxicol Appl Pharmacol. 2012 Sep 27;265(1):113–121. doi: 10.1016/j.taap.2012.08.037

Figure 3. Pre-treatment effects of DZP, KET, and MK-801 on TMDT syndrome.

Figure 3

3A. Number of clonic seizures (mean ± S.E.M.) in mice injected with 0.4 mg/kg TMDT and one of the following: vehicle (controls), DZP 1.0 or 5.0 mg/kg, KET 35 mg/kg or MK-801 1.0 mg/kg. Pre-treatment (15 min prior to TMDT injection) with KET increased the number of clonic seizures (*p<0.05; Kruskal-Wallis test). Treatment with 5.0 mg/kg of DZP completely blocked any motor activity, including clonic seizures.

3B. Latency to onset of clonic seizures (mean ± S.E.M.) induced by administration of TMDT 15 min after each drug pre-treatment. Only DZP 1.0 mg/kg was effective in delaying seizures (*p<0.05; ANOVA with post-hoc Dunnet’s test; n/a – not applicable, there were no seizures).

3C. Number of tonic-clonic seizures (mean ± S.E.M.) in mice injected with 0.4 mg/kg TMDT 15 minutes after each pharmacological pre-treatment. While DZP 5.0 mg/kg completely suppressed seizures and ketamine moderately increased their occurrence, Kruskal-Wallis test did not return any significant differences.

3D. Kaplan-Meier analysis of latency to onset of tonic-clonic seizures in mice injected with 0.4 mg/kg TMDT for each pharmacological pre-treatment. Neither DZP 1.0 mg/kg nor KET 35 mg/kg pre-treatment affected latency to onset of tonic-clonic seizures.

3E. Kaplan-Meier analysis of latency to death in mice injected with 0.4 mg/kg TMDT for each pharmacological pre-treatment. Neither DZP 1.0 mg/kg nor KET 35 mg/kg pre-treatment had any effect.