LOCAL DISTURBANCE OF NEURONAL MIGRATION IN THE S-100-BETA-RETARDED MUTANT MOUSE

Homozygotes of a mouse strain with genetic polydactyly (Pdn) show disr upted cortical lamination and a significant decrease of S-100 beta-imm unoreactive elements in a particular area of the brain. In order to un derstand the abnormal cortical formation at the cellular level, the mi gration of cortical neurons and the develop ment of glial cells were s tudied using bromodeoxyuridine (BrdU), S-100 beta, and glial fibrillar y acidic protein (GFAP) immunohistochemistry. Homozygous mice (Pdn/Pdn ) displayed a variable pattern of abnormalities. Irregular GFAP-positi ve radial glial cells and disturbance of neuronal migration were found in a circumscribed area of the caudo-dorsal cortex of newborn Pdn mou se. The number of S-100 beta-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 glial cells, especially a significant decrease of S-100 beta-immunore active cells.