NEURONAL CIRCUIT FORMATION IN THE GENETICAL AND EXPERIMENTAL BRAIN MALFORMATION ANIMAL.

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Homozygote of a mouse strain with genetic polydactyly (Pdn) show disrupted cortical lamination and significant decrease of S-100beta immunoreactive elements in a particular area of the brain. In order to understand the abnormal cortical formation at the cellular level, migration of cortical neurons and development of glia cells were studied using bromodeoxyuridine (BrdU), S-100beta and glial fibrillary acidic protein (GFAP) immunohistochemistry. Homozygous mice (Pdn/Pdn) displayd a variable pattern of abnormalities. Irregular GFAP-positive radial glia cells and disturbance of neuronal migration were found in a circumscribed area of the caudo-dorsal cortex of newborn Pdn mouse. The number of S-100beta-positive cells was reduced in this area. The present results suggest that abnormal cortical lamination closely correlates with disturbance of neuronal migration and abnormalities of glia cells, especially a significant decrease of S-100beta immunoreactive cells.