Experimentally induced focal microgyria and status verrucosus deformis in rats — Pathogenesis and interrelation histological and autoradiographical study
Tóm tắt
Experiments with neonatal rats were used to investigate the problem of pathogenesis of microgyria and status verrucosus deformis. A.A Microgyric Four Layered Cortex was induced by contact freezing (Dvorák and Feit, 1977). The Golgi-Cox method, paraffin-wax sections and H3 thymidine autoradiography were used in a series of four experiments with the following results: (1) Indications of 6-layered lamination were found in a 4-layered microgyric cortex produced during the period of neuroblast migration; (2) Migrating neuroblasts were deployed according to the “inside out” rule in regions of partial necrosis and those surrounding total necrosis similar in pattern to that seen in the undamaged cortex; (3) Neuron losses arising from focal necrosis were not compensated for by reparative mitotic activity (either in loco or in the germinative zone); (4) Focal necrosis in 4-day-old (after neuroblast migration had finished) formed a defect which was healed with the participation of glia. A microgyric cortex was at this stage no longer formed. The findings show that indications (traces) of 6-layered lamination in 4-layered microgyric cortex need not always be a residual state of pathologically changed, previously formed lamination. Microgyric 4-layered cortex can also arise from damage to the cortex during the period of neuroblast migration. B.Morphological Features Similar to Changes in Status Verrucosus Deformis (superficial nodules, micropolygyric nodules, shallow microsulci, intracortical nodules) occured in rats after cumulative focal necrosis affecting only the surface regions of the cortex (duration of freezing 1–2 s, in the case of microgyric cortex 2–3 s). These features appeared because of the migration of neuroblasts through partial necrosis and in the region surrounding total necrosis, by the mechanism similar to that in experimental microgyria. The possibility that status verrucosus deformis arises in the second half of the migration period and the mechanism of the formation of cell protrusions in the molecular layer are discussed.
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