Figure 1.

H&E staining, and MAP2, laminin (green fluorescence) and GFAP (red fluorescence) immunoreactions. In panel (a) H&E staining shows the WT lissencephaly, while the altered phenotype is shown in panel (b). In the cerebral cortex, MAP2 immunoreaction (insets of a and b, arrows) evidences the run of neuron dendrites and their positioning. Laminin immunopositivity highlights differences of cortical meningeal BM between WT (c and inset) and altered phenotype (d and inset). The WT cerebellum morphology is illustrated in panel (e), while the altered phenotype in panel (f), where the insertion points to the abnormal vascularization (asterisk), ectopic cells (arrowhead) and absence of granule cells (arrow). In the cerebellum, laminin immunopositivity brings out BM as a continuous layer in WT and small blood vessels within the molecular layer (g). The altered phenotype displays cortical abnormality with lack of BM and large blood vessels penetrating the molecular layer (h). GFAP immunopositive fibers and their endfeet are shown to reach the cerebellar surface only in WT (red fluorescence in the inset of panel g, arrowhead), while in altered phenotype (inset in h, arrowhead) they are disorganized and the endfeet are not detectable. In panels (c, d, g, h) nuclei are counterstained with Hoechst 33258 (blue fluorescence). Altered phenotype, dal/+and dal/dal, mice; Hi, hip-pocampal formation.