To investigate the mechanisms of radial and tangential
neuronal migration disorders, immunohistochemical expressions of reelin,
vimentin, and
calretinin were examined in brain lesions induced by ibotenate (an agonist of the
N-methyl-D-aspartate [
NMDA] complex receptor) in hamsters. Thirty-four newborn hamsters were subjected to intracerebral
injections of ibotenate, and 12 animals served as the control. These hamsters were examined at 1, 2, 3, 5, and 7 days after
injections. The cortical lesions observed after ibotenate
injections had a strong resemblance to the following
neuronal migration disorders: (1) microgyria, (2) focal subcortical heterotopia, and (3) leptomeningeal glioneuronal heterotopia. In microgyria, the radial glial fibers were sparsely distributed, but in leptomeningeal glioneuronal heterotopia,
vimentin-positive fibers extended into this abnormal neural tissue.
Calretinin-immunoreactive neurons and fibers were present along the lesion forming the microgyria and abnormal neuronal arrangement. Focal subcortical heterotopia also included a small number of
calretinin-expressing neurons originating from the subplate neuronal population. These results imply that the
neuronal migration disorders produced by ibotenate show not only the migrational arrest of neurons but also interference from the termination of the migration process. We also suggest that the heterotopic neurons constituting the focal subcortical heterotopia originate in the lateral or medial ganglionic eminence of the ventral telencephalon, probably caused by the abnormal tangential neuronal migration.