Experimental neuronal migration disorders following the administration of ibotenate in hamsters: the role of the subventricular zone in the development of cortical dysplasia.

To examine the role of subventricular zone in cortical dysplasia, an experimental model was established using a neuronal tracing study. Ibotenate is a glutamate receptor agonist, and its intracerebral injection produces excitotoxic lesions mimicking microgyria and heterotopia. A total of 72 newborn hamsters were subjected. Biotinylated dextran amine was injected into the ganglionic eminence for the neuronal tracer. The cortical lesions and apoptotic cells were analyzed. In the microgyric cortex, terminal deoxynucleotidyl transferase-mediated 2' -deoxyuridine 5'-triphosphate-biotin end labeling-positive cells were increased and accumulated in the cortical folding. Biotinylated dextran amine-positive cells and fibers were derived from the dorsolateral subventricular zone and directed toward the cortical folding. In the heterotopic cortex, terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate- biotin end labeling-positive cells were distributed around the heterotopia, but number of cells was not remarkable. Our findings suggest that the subventricular zone plays an important role in the formation of cortical dysplasia, especially in the microgyria, after excitatory neuronal injury.