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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Exp Neurol. 2012 Jul 5;237(2):346–354. doi: 10.1016/j.expneurol.2012.06.029

Figure 6. Inhibition of miR-184 increases seizure-induced neuronal death in epileptic tolerance.

Figure 6

Mice received Scr or Ant184 (0.5 nmol i.c.v.) then 24 h later epileptic tolerance (Tol) was modelled by first subjecting mice to seizure preconditioning (15 mg/kg KA, i.p.) followed 24 h later by SE induced by intra-amygdala KA. (A) Electrographic seizure parameters recorded for 40 min after triggering SE in seizure preconditioned mice (n = 6–8 per group). (B) Representative spectrogram of EEG frequency and amplitude data during the 40 min after triggering SE. (C) Photomicrographs showing FJB staining in the ipsilateral hippocampus 24 h after SE in seizure preconditioned mice that received Scr or Ant184. Dead neurons (black dots) are more abundant in area CA1, while both CA3 and hilus are similarly injured (arrows). Scale bar, 650 μm. (D) Graphs showing ipsilateral FJB counts 24 h after SE in seizure preconditioned mice given either Scr or Ant184 (*p < 0.05 vs. Scr; n = 6–8 per group).