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. 2016 Mar 21;18:e4. doi: 10.1017/erm.2016.3

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© Cambridge University Press 2016

This is an Open Access article, distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike licence (http://creativecommons.org/licenses/by-nc-sa/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the same Creative Commons licence is included and the original work is properly cited. The written permission of Cambridge University Press must be obtained for commercial re-use.

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Figure 6. — Effect of miR-124 on CREB1 activity in the hippocampus. (a) Sample Western blots of NMDAR1 in normal (without seizure inducing) and model rats (PTZ-induced seizure in rat models) without treatment (control), and in animals treated with mimics control and mimics. (b) Summary of the relative NMDAR1 analysed from h. ▼P > 0.05, compared with the normal, n = 4. (c, d) Immunoprecipitation was used to survey the binding status between CREB1 and NMDAR1 or GLUR1. (e, f) Immunohistochemistry images show strong (e, 24 h after pilocarpine-induced seizures) and weak (f, control group) immunoreactive staining of pCREB in the dentate gyrus. Scale bar, 200 µm. (g) Sample Western blots of pCREB before (normal) and at different time points of pilocarpine-induced seizure. (h) Summary of pCREB activity showing a significant increase after seizures. *P < 0.05, n = 5. (i) Sample Western blots of pCREB in normal (without seizure inducing) and seizure rats without treatment (control), and in rats treated with mimics control and mimics. (j) Summary of the relative pCREB analysed from I. *P < 0.05, compared with the normal. ▲P < 0.05, compared with the mimics control, n = 5. (k) Relative CREB1 mRNA levels in normal (without seizure inducing) and seizure rats without treatment (control) and in animals treated with mimics control and mimics. *P < 0.05, compared with the normal. ▲P < 0.05, compared with the mimics control, n = 5.

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