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.