Brain dysplasia evoked by gamma irradiation at different stages of prenatal development leads to different tonic and clonic seizure reactivity.

Rats with brain dysplasia evoked by interruption of different stages of prenatal neurogenesis show characteristic variations in susceptibility to seizures depending on the neurochemical specificity of pharmacological agents used to evoke seizures. To verify a discrepancy between the data obtained using different pharmacological models, neurochemically neutral electroshocks were applied here. To produce brain dysplasia of different degrees, pregnant Wistar rats were exposed to a single 1.

Brains with different degrees of dysplasia show different patterns of neurodegenerative changes following pilocarpine-induced seizures. Histologic evidence of tissue damage correlated with MRI data.

Objective: Brain dysplasias produced by irradiation with gamma rays at various stages of prenatal development cause different post-natal susceptibility to seizures. To detect possible determinants of this difference, patterns of degenerative changes in the dysplastic brains following pilocarpine-induced epilepsy were analysed.

Methods: Pregnant Wistar rats were exposed to a 1.

Congenital brain dysplasias of different genesis can differently affect susceptibility to pilocarpine- or kainic acid-induced seizures in the rat.

Interruption of neurogenesis and/or neuronal migration produces brain dysplasia modifying susceptibility to epileptic seizures in adulthood. The course of neurogenesis has a strictly defined time-table. Consequently, the developmental stage at which the interruption occurs determines what functional subsystem potentially involved in epileptogenesis will suffer from irreversible neuronal deficit.