Exploring The Mechanism Of The Effects Of Cerebral Ischemia On The Susceptibility To Seizure

Epilepsy is one of the common chronic cerebral diseases. The epidemiological studies have identified that the prevalence rate here in China is about 5‰-7‰.All-kinds of cerebral diseases could induce epilepsy and the incidence is around 10%. In the senile epilepsy, about 30%-44% of the cases were caused by cerebrovascular disease. And 7.5%-12.5% of late epilepsy is caused by cerebral disease. In some cerebral ischemia diseases, epilepsy is possibly the only or the first symptom. In order to explore the cellular mechanism of epilepsy after cerebral ischemia more deeply, the rat model was established by the modified intraluminal thread method of occlusion and reperfusion in right middle cerebral artery (MCA) , and followed by chronically induced seizure with sub-dosage of pentylenetetrazol ( PTZ, 35mg/kg, i.p.) . Behaviors were then investigated and recorded on rats model to evaluate the changes in susceptibility to seizure, as well the changes in neuropathology and immunoreactivity ( IR) of glia fibrillary acidic protein ( GFAP ), neuropeptide Y( NPY)and cholecystokinin(CCK)in sub-regions of rat brain by thionine-staining and immunocytochemistry (ICC).The results demonstrated that, 20 days after successful PTZ kindling, the group of ischemia was easier to be kindled than the group of sham apparently; the stages of seizure were higher at the same time. Loss of pyramidal cells at CA1 and CA3 occurred on rightside of dorsal hippocampus, as well as neurons in frontal cortex(Fr). Meanwhile, GFAP immunoreacitive astrocytes were presented markedly, with larger cell bodies, thicker and longer protrusions and stronger staining in Fr, CA1 and hilus. Loss of NPY-IR positive interneurons and increase of CCK-IR positive interneurons occurred on right side of dorsal hippocampus, as well as neurons in Fr. Moreover, NPY-IR increased and CCK-IR decreased.These results indicate that, the enhancement in susceptibility to seizure in rats with cerebral ischemia is closely related to the neuron loss in Fr, CA1, CA3,and the proliferation of astrocytes in Fr, CA1, hilus. Epilepsy caused by cerebral ischemia accelerates the sclerosis of hippocampus. Loss of NPY-IR positive interneurons and increase of CCK-IR positive interneurons, correspondingly, NPY-IR increased and CCK-IR decreased in dentate gyrus cells(DGC) and hilus on right side of dorsal hippocampus, as well as neurons in Fr, which may involve the mechanism of the enhancement in susceptibility to seizure after cerebral ischemia.