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.

Research paper by Z Z Setkowicz, K K Majcher, D D Janicka, Z Z Sułek, T T Skórka, A A Jasiński, K K Janeczko

Indexed on: 09 Jun '06Published on: 09 Jun '06Published in: Neurological research


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.Pregnant Wistar rats were exposed to a 1.0 Gy dose of gamma rays on gestation days 15 (E15) or 17 (E17). On post-natal day 60, their offspring received pilocarpine injections to evoke status epilepticus. Motor manifestations of seizure activity were observed continuously for 6 hours and rated. Six days following the status epilepticus, the rats were anesthetized and T(2)-weighted magnetic resonance (MR) images were obtained. Frontal sections of the brains were immunostained for immunoglobulins G (IgGs) to detect blood-brain barrier damage and IgG cell uptake and glial fibrillary acidic protein (GFAP) or S-100-beta protein to visualize astrocytes. Bandeiraea simplicifolia isolectin-B4 (BSI-B4) isolectin histochemistry was also performed to detect microglia/macrophages.Tissue damages within epileptic brains as observed by light microscopy generally reflected changes in magnetic resonance imaging (MRI) at similar locations. Brains of rats irradiated on E15 or E17 and showing epileptic symptoms at comparable intensity also displayed different distribution of the pathologic changes. Among other post-epileptic changes, in rats irradiated on E17 as well as controls, the laterodorsal and ventrolateral thalamic nuclei showed signs of severe degeneration. In rats irradiated on E15, the nuclei were free of such changes.The obtained data point to important differences in the pattern of propagation of epileptic activity in the dysplastic brains suffering from neuronal loss in functionally different structures.