| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
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 in hamsters. The cortical lesions observed after ibotenate injections had a strong resemblance to the following neuronal migration disorders ; (1) microgyria, (2) subcortical nodular heterotopia, and (3) leptomeningeal glioneuronal heterotopia. In microgyria, the radial glial fibers were sparsely distributed, but in leptomeningeal glioneuronal heterotopia, vimentin-positive fibers invaded this abnormal neuronal tissue. Calretinin-immunoreactive neurons and fibers were present along the lesion forming the microgyria and abnormal neuronal arrangement. Subcortical nodular heterotopia also included a small number of calretinin-expressing neurons originated from the subplate neuronal population. These results imply that the neuronal migration disorders produced by ibotenate show not only the migration arrest of neurons, but also interference from the termination of the migration process. We also suggest that the heterotopic neurons constituting the subcortical nodular heterotopia originate in the lateral or medial ganglionic eminence of the ventral telencephalon, probably caused by the abnormal tangential neuronal migration.
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