Abstract
Abstract : Our lab developed an animal model to elucidate factors associated with abnormal neocortical development and to attempt repair of cortical dysgenesis. We disrupt corticogenesis using an anti-mitotic methylazoxy methanol (MAM), which inhibits mitosis for several hours. The effects of MAM on neocortical development are assessed during early (embryonic day 24; E24) and late (E33) corticogenesis in ferrets. These animals have protracted cortical development with neurogenesis and migration continuing postnatally. MAM treatment on E24 leads to disorganized cortical laminae, abnormal radial morphology, precocious differentiation of radial glia, and dispersal of Cajal Retzius cells. MAM treatment on E33 leads to less severe effects including diminished layer 4, widespread termination of thalamocortical afferents, and abnormal distribution of GABAA-alpha receptors.
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