miRNA biogenesis components in neocortex and in experimental epilepsy.

<p>(A) Representative Western blots showing expression of Dicer, Drosha and AGO2 in neocortex samples from TLE patients (TLE 9–11) and controls (C3–C5). (B) Graphs (<i>n</i> = 3 per group) showing semi-quantification of levels of each protein. **<i>p</i><0.05 compared to controls. Protein levels corrected to α-Tubulin (α-Tub). (C) Representative immunohistochemistry illustrating the hippocampal damage in epileptic mice. (a) Field view (4× lens) showing triple-stained section from an epileptic mouse 21 days after status epilepticus. Box highlights main lesion area in CA3. <i>b,c</i> are 20× lens field views of the lesioned CA3 area showing reduced NeuN (red) and increased GFAP (green) staining. (D) Representative views of the CA3 from a control mouse at 21 days which did not undergo status epilepticus. <i>a–c</i> show NeuN (red), GFAP (green) and a merge of these with DAPI overlay. Note the intact neuron population and minimal GFAP staining. Scale bar in C<i>a</i>, 500 µm; C<i>b</i>, and D<i>a</i>, 100 µm. (E, F) Representative Western blots (<i>n</i> = 1 per lane) showing protein levels of NeuN, GFAP, Dicer, Drosha and Ago2 in CA3 samples from control and epileptic (21 day) mice (TLE-HS). (G) Graph quantifying reduction in hippocampal CA3 Dicer levels in epileptic animals (<i>n</i> = 7–8 per group; *<i>p</i><0.05 compared to control). Protein levels corrected to α-Tub. (H) Representative Western blots (<i>n</i> = 1 per lane) show non-damaging seizures do not cause a reduction of Dicer levels. α-Tubulin is included as a guide to protein loading.