Pathogenetic basis of seizure susceptibility in a hamster model of cortical malformation

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Sustained elevation of the intracellular level of Ca2+ in response to glutamate receptor activation can result in depolymerization of microfilaments and microtubules, thus leading to dendritic outgrowth cessation and regression. These processes are suggested to be the primary mechanisms underlying the neuronal migration disorders and the resultant polymicrogyria observed in this experiment. A neuronal tracing study of progenitor cells in the ganglionic eminence using biotinylated dextran amine (BDA) demonstrated the interneurons to be mobilized to the microgyric area out of the ganglionic eminence, thus suggesting the development of new inhibitory neuronal connections after the onset of excitotoxic brain lesions. The lateral paramicrogyral area had the greatest number of parvalbumin-immunoreactive neurons, which was increased significantly in comparison to that in the control cortex (P < 0.01). We suggest that the callosal, thalamic and intracortical afferents to the microgyrus and paramicrogyral area may induce a remarkable imbalance between the excitatory and inhibitory activities of the cortical structures, associated with the epileptogenic mechanism in polymicrogyria.