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. 2013 Oct 2;8(10):e76299. doi: 10.1371/journal.pone.0076299

Figure 7. Effect of DNA methylation inhibitor RG108 on KA induced DNA methylation of the gria2 5’ region and epileptiform bursting 1 week following a transient 2 hour exposure.

Figure 7

(A) Methylation differences between control (Ctrl, n=4 technical replicates on 3 different mice of origin), KA treated (KA, n=4 technical replicates on 3 slices from different individual mice), RG108 (RG108 n=4 technical replicates on slices from 2 different mice) and RG108 and KA treated slices (RG108+KA n=4 technical replicates on 2 different mice of origin) 1 week after removal of the drug and incubation in drug free medium. (B) Sample neurons’ membrane potentials recording in current-clamp mode of Ctrl, KA, RG108 and RG108 + KA treated samples. (C) Average spontaneous bursting activity of hippocampus slices after treatment with the different drugs. Significant increase in bursting activity can be observed in KA treated slices (n=19) vs. control (n=16). RG108 combined with KA treatment (RG108+KA, n=14) blocks the spontaneous bursting induces by KA treatment (n=19). Treatment with RG108 alone (n=12) does not have any significant effect on bursting compared to control slices (n=16). Significance between the different conditions in multiple-comparisons was calculated using Student t-test with Holm-Bonferroni correction for multiple comparisons. (D) Correlation between bursting frequency and average probe methylation levels in all the treatments samples (n=12) (Ctrl, KA, RG108 and RG108 + KA) (p=0.003, Pearson’s r=0.7763). * p<0.05 ** p<0.01 *** p<0.005.