The extracellular matrix and diffusion barriers in focal cortical dysplasias (pages 2017–2024)
Josef Zamecnik, Ales Homola, Michal Cicanic, Klara Kuncova, Petr Marusic, Pavel Krsek, Eva Sykova and Lydia Vargova
Article first published online: 26 APR 2012 | DOI: 10.1111/j.1460-9568.2012.08107.x
NeuN immunohistochemistry revealed a normal laminar distribution of neurons in non-malformed cortex (A) and the delamination and columnar disorganization of neurons in FCD type I (B), which was accompanied by the presence of large dysmorphic neurons with atypical morphology and aberrant orientation in FCD type II (C). Immunostaining with anti-GFAP demonstrated only scarce GFAP-positive glial cell processes, mostly in the subpial zone of the non-malformed cortex (D). The number and branching of GFAP-positive cell processes were increased in FCD type I (E), and further increased in FCD type II (F). Scale bars: (A) 500 lm, (B and C) 200 lm, and (E and F) 100 lm. Representative TMA+-diffusion curves recorded in each distinct type of tissue sample with the corresponding values of the ECS diffusion parameters a, k and k% are given below. The disrupted cytoarchitecture and ECM composition slows down the diffusion in the ECS of FCD type I, as reflected by an increase in k. In FCD type II, a is larger; however, k is also increased, indicating that diffusion is also slowed down. For comparison, a ‘normal’ TMA+-diffusion curve (grey silhouette) is superimposed on the diffusion curve recorded in the dysplastic tissue.