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Disruption of neuronal migration in LCMV-infected brain

Congenital LCMV infection disrupts neuronal migration in the developing human brain and in the rat model. [A] MRI scan of a 3-year-old child with congenital LCMV infection. The MRI scan demonstrates microencephaly and a deficit of white matter (arrowheads) with a compensatory enlargement of the lateral ventricles (asterisks). There is also a diminished number of cortical sulci and an abnormally smooth cortical surface (white arrow). This is strongly suggestive of pachygyria, a developmental defect due to abnormal neuronal migration. [B] Two-micron-thick section through the normal cerebellar cortex of control (uninfected) adult rat demonstrating the trilaminar cytoarchitecture of the cortex, which consists of the molecular layer (M), Purkinje cell layer (P), and granule cell layer (G). Within the molecular layer, a few stellate cells and basket cells (arrowheads) are normally present. In contrast, granule cells (arrows) have migrated through the molecular layer to the granule cell layer. Granule cells no longer reside in the molecular layer in the normal cerebellum. [C] Two-micron-thick section through the cerebellar cortex of an adult rat infected during early postnatal life with LCMV. Many granule cells (arrows) remain abnormally placed within the molecular layer. As a result of LCMV infection, these neurons have failed to migrate properly to their normal location within the granule cell layer and remain permanently ectopic within the molecular layer. Magnification bars represent 100 um in B and C. (Part of this figure is reproduced from Bonthius and Perlman, PLoS Pathogens 2007; 3:1541-50.)

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