ABSTRACT
BACKGROUND: The recurrent temporal lobe epilepsy induces contralateral cell damage and secondary epileptogenesis in the contralateral hippocampus of rats. This phenomenon is fairly constant and has been used as a model of human temporal lobe epilepsy. It is necessary to understand this patho-mechanism in order to prevent this cell damage. METHODS: We have investigated the patho-mechanism of secondary epileptogenesis by using the rat model injected with kainic acid (KA) into the unilateral hippocampus. KA model shows initial complex partial seizures originating from the limbic structures and following convulsive status epilepticus. Immunohistochemical staining for c-fos expression, TUNEL stain for apoptosis, and hematoxylin-eosin (H-E) stain for morphologic changes were used. RESULTS: In the injected hippocampus, transient activation of c-fos was expressed in the dentate gyrus and CA3 hippocampal area, which were shaded out within 24 hours after the onset of limbic seizure. The stained cell with normal appearance was not observed in the H-E stain after 72 hours due to diffuse cell death. In the contralateral hippocampus, transient expression of c-fos was observed in the dentate gyrus, hilus, CA3, and CA1 area. But the expression of c-fos in the CA3 and CA1 area was sustained to 24 hours. Cell loss was mild in the CA3 and hilus, and mild cell degeneration and shrinkage were observed in the CA1 area. Apoptotic body was expressed in the CA1 area at 72 hours after the onset of seizure. CONCLUSION: These results mean that the area of prolonged expression of c-fos is vulnerable to apoptosis. Also it suggests that the patho-mechanism of ipsilateral hippocampus is an acute cytotoxic edema, whereas the contralateral damage is an apoptosis.
Subject(s)
Animals , Humans , Rats , Apoptosis , Cell Death , Dentate Gyrus , Edema , Epilepsy, Temporal Lobe , Hippocampus , In Situ Nick-End Labeling , Kainic Acid , Models, Animal , Neurons , Seizures , Status EpilepticusABSTRACT
No abstract available.