LIC inhibition severely impairs neuronal migration at post-natal stages. (A and B) E16 rat brains were in utero electroporated with control vector or shRNAs for LIC1 or LIC2. Analysis was done 2 wk after injection, at P7. Brain slices were stained for the mature neuronal marker, NeuN. The CP was equally divided in bins for quantifications purposes. (A) Images of the post-natal neocortex across conditions. Bar, 200 µm. (B) Quantification of the distribution of cells through the white matter and the CP. Data are presented as mean ± SD in B, and unpaired t test was used (*, P < 0.05; **, P < 0.01). Data in B include at least 1,215 cells from at least four pups, per condition. (C) Schematic illustration showing LIC roles in neocortical development. In yellow, RGPs undergoing INM. In green, multipolar post-mitotic neurons become bipolar and migrate to the CP. LIC1 participates in the apical nuclear migration of RGPs (a), the multipolar to bipolar transition (b), and glial-guided migration (c). LIC2 had no significant function in the previous behaviors, but plays an essential role in TST of neurons (d). WM, white matter.