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. 2017 Feb 15;7:42491. doi: 10.1038/srep42491

Figure 2. Role of PDI in seizure activity in response to PILO.

Figure 2

(A) Western blot of PDI protein expression level in control siRNA- and PDI siRNA-infused animals 3 days after S.E.M., molecular weight marker. (B) Quantification of PDI expression level 3 days after SE (mean ± S.E.M.; *, #p < 0.05 vs. control siRNA and non-SE animals, respectively; n = 7, respectively). PDI siRNA effectively decreases PDI protein expression level in the hippocampus. (C–E) Effect of PDI siRNA on seizure susceptibility in response to PILO. PDI knockdown reduces seizure susceptibility and its severity in response to PILO. (C) Representative EEG traces and frequency-power spectral temporal maps in response to PILO. (D,E) Quantification of effect of PDI siRNA on SE induction, latency and total EEG power in response to PILO (mean ± S.E.M.; *p < 0.05 vs. control siRNA; n = 30, respectively). (F–H) Effects of DTNB and bacitracin on seizure susceptibility in response to PILO. DTNB and bacitracin also decreases seizure susceptibility in response to PILO. (F) Representative EEG traces and frequency-power spectral temporal maps in response to PILO. (G,H) Quantification of effects of DTNB and bacitracin on SE induction, latency and total EEG power in response to PILO (mean ± S.E.M.; *p < 0.05 vs. vehicle; n = 10, respectively).