Mechanism of Neuron Injury of Rats with Kainite Acid-Induced Epilepsy / 实用儿科临床杂志

ABSTRACT

Objective To investigate the dynamic changes of glutamic acid(Glu) levels,ATP levels,free calcium ion,mitochondrial membrane potential,apoptosis related to mitochondrial pathways of apoptosis and Na+-K+-ATPase activity,and explore the mechanism of mitochondrial pathways of apoptosis in neuron injury of rats with kainite acid(KA)-induced epilepsy.Methods KA-induced epilepsy model was induced by injection of KA into the hippocampus.Forty SD rats were randomly divided into 2 groups control group(n=8)and KA group(6 h,1 d,3 d,7 d,n=8).The concentration of Glu in hippocampus CA3 area was detected by high performance liquid chromatography.The apoptosis of hippocampus neurons and the concentration of Ca2+ were assayed by flow cytometry.The mitochondrial membrane potential was detected by JC-1.The Na+-K+-ATPase activity was examined.Results 1.The concentration of Glu in hippocampus increased at 3 d after KA injection and reached the peak after 7 d injection.2.The concentration of Ca2+ level,mitochondrial membrane potential,and the number of apoptosis neurons were significantly increased,wherase the mitochondrial membrane potential decreased after 6 h of KA injection,7 d after KA injection,and the changes were more severe.3.In the hippocampus,the activities of the Na+-K+-ATPase significantly decreased at 1 d after KA injection,and they decreased more over at 7 d after KA injection.4.The levels of ATP,mitochondrial membrane potential,and the activity of the Na+-K+-ATPase were negatively correlated with the neuron apoptosis(Pa