NPY,Caspase-3 Expression In Hippocampus And In Cortex Of Rat Model Of Temporal Epilepsy During Different Periods And Effected By VPA And NGF

Object: This paper is a study of rat model of temporal epilepsy. An animal model of chronic temporal lobe epilepsy caused by kainic acid (KA) was established. The pathogenesis of this drease as a focus was studied in view of neurology and neurochemistry. The pathologic change and therapeutic effect of drug were observed. The pathogenesis and pathopoiesis of this model was studied. Method: 0.8ug/0.2ul of KA was microinjected into hippocampal posterior abdomen of Wistar rat via stereotaxic technique, resulted in local epilepsy focus. Video examination for observation of the symptom, deep EEG was carried out, and then the rats were killed at different periods of time, the brain tissues were extracted from the rats. Then radioimmunoassay was carried out. The neuropeptide Y (NPY) expression in temporal lobe epilepsy model was studied quantitatively. The NPY expression in hippocampus and in cortex of this model at different periods of time were observed by this immunohistochemical method. Apoptosis close related cysteine proteinase-caspase-3, of which expressions were also studied in different brain areas, in different periods of time. Results: 1. The chronic temporal epilepsy model caused by KA wasestablished. The model was proved by EEG and behavior studies. Localized epilepsy expression was seen immediately after injection of KA, and it developed to tonic-clonic seizure. In chronic stage there was a repeated spontaneous attack and it continued . In acute and chronic stages there were typical epilepsy attack as well as intermediate stage expression in EEG.2. The level measurement of NPY by radioimmunoassay showed. In the group, which was not caused epilepsy, there was certain content of NPY. The NPY level reduced 2hr after KA injection. The NPY level increased gradually with the time, and it continued for a period of time. The NPY level was higher in hippocampal area than in cortex. After administration of valproic acid (VPA) elevated levels of NPY were found both in hippocampus and in cortex. However after administration of exogenous nerve growth factor (NGF) no observable change of NPY level was found.3. The results of NPY expression study by immunohistochemical method: The NPY expressions in hippocampus were most significant in CA1, CA3 and in hilus area of dentate gyms. In other areas of hippocampus the NPY expressions were found in cortex..4. The results of caspase-3 expression study by immunohistochemicalmethod: Low caspase-3 expression in normal rat brain. 2hr after KA injection the caspase-3 expressions in hippocampus and in cortex increased sharply and it continued for a period of time. Finally, the caspase-3 expression decreased, but still higher than normal rat. Hewever the caspase-3 expression was still very high in cortex. Conclusion: In KA model the hippocampus amygdala plays a key role in epilepsy. Therefore it provides a mimic optimal conditions for human temporal lobe epilepsy study. It's an effective method of studying the development, change and pathopoiesis of epilepsy. There is a close relationship between NPY and epilepsy. The regulation of NPY via VPA may be one of the antiepilepsy mechanism of mechanism of VPA. Moreover NGF can enhance the caspase-3 expression. Excito-amino acid can aggravate the apoptosis, which may be one of the reason for intractability of epilepsy.