Abstracts

Rationale: The epileptic activity from hippocampal formation is spread to the rest of the brain during temporal lobe epilepsy (TLE). In this condition, sprouting of mossy fibers, gliosis and cell death take place in the hippocampal region. However which of these neuropathological changes responsible for triggering seizure and epileptic discharge remains unknown. C57BL/6 mice were reported to be “resistant” to hippocampal damage after seizure induced by systemic injection of kainic acid, even though these mice are susceptible to epileptogenesis and status epilepticus responses. Astrocytes participate in neurogenesis, synaptogenesis and synaptic modulation. Also, these cells maintain the glutamate homeostasis, where its inhibition leads to a seizure prone state. Methods: We have studied here cellular elements of the hippocampal and neocortex from adult male C57BL/6 mice after seizure induced by kainic acid (KA, single doses= 30mg/kg, intraperitoneal; saline injection was used as control). Behavior and EEG activity from hippocampus was recorded within 2 hours after KA injection. Brains were dissected and processed using silver stain, nissil, tunel staining and IR of GFAP, neurofilament, parvalbumin and myelin basic protein analysis at 24 hours and 30 days after KA injections. Progression of seizure complexity was observed after KA injection.Results: Our results indicate preservation of CA1, CA3 and DG neurons, gliosis and the appearance of non-tunel positive cells after 24 hours and 30 days of generalized seizures in hippocampus. There is a reduction of neurofilaments, loss of interneuron and oligondendrocytes cells and enhanced gliosis in the neocortex after 30 days after KA injection. Conclusions: We postulate that loss of cortical inhibition takes place and demyelization is activated during kainic acid induced epileptogenesis.