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Fig. 1 | Molecular Autism

Fig. 1

From: Rescuing epileptic and behavioral alterations in a Dravet syndrome mouse model by inhibiting eukaryotic elongation factor 2 kinase (eEF2K)

Fig. 1

Scn1a ± mice exhibit higher levels of eEF2 phosphorylation in total homogenate of hippocampus and cerebral cortex compared with WT mice and eEF2K deletion modulates the expression of a set of proteins that regulate GABAergic synaptic transmission. A,B Representative western blots and relative quantification for phosphorylated eEF2 in samples from hippocampus (A) and cerebral cortex (B) in 3, 6 and 9 months old Scn1a ± and WT mice. 3 months: hippocampus and cerebral cortex WT n = 8, Scn1a ± n = 9; 6 months: hippocampus WT n = 4, Scn1a ± n = 10, cerebral cortex WT n = 4, Scn1a ± n = 8; 9 months hippocampus and cerebral cortex WT n = 5, Scn1a ± n = 5. All Data are presented as mean ± SEM. Statistical analysis *p < 0.05 versus corresponding WT; One-sample t-test. C,D Representative western blots and relative quantification show expression levels of Synapsin 2b (C) and GABAARα5 (D) in total homogenate of hippocampus (left) and cerebral cortex (right) from 3 months old WT, Scn1a ± eEF2K−/−, Scn1a ± and eEF2K−/− mice. All data are presented as mean ± SEM. N = 7 per group for Synapsin 2b. N = 6 per groups for GABAARα5. Statistical analysis *p < 0.05 versus corresponding WT, $p < 0.05 versus corresponding Scn1a ± ; One-simple t-test

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