ABSTRACT
Epilepsy is common clinically, which is a type of chronic disease.It is a transient brain dysfunction caused by sudden abnormal discharge of brain neurons.At present, there is still some controversy about the etiology of epilepsy.With the deepening of clinical researches on epilepsy, genetic and biological studies have shown that mutations in genes encoding ion channels in the nucleus of neurons may lead to changes in membrane channel proteins and changes in channel properties and structures are closely related with epilepsy.Sodium-controlling channel proteins play a very important role in epilepsy.They can control the changes of cell currents by turning them on and off to regulate the discharge of brain neurons.This review mainly discussed the correlation between the SCN9A gene encoding sodium ion channel Nav1.7 and the onset of epilepsy.
ABSTRACT
Objective To investigate the expression of excitatory neurotransmitter glutamate (Glu),inhibitory neurotransmitter gamma-aminobutyric acid (GABA),glutamate receptor R1 (GluR1) and gammaaminobutyric acid receptor A (γ-aminobutyric acid A receptor,GABAA) in the brain of rats with intrauterine growth retardation.Methods Thirty-two healthy Wistar female virgin rats and eight healthy Wistar male rats were purchased from the Laboratory Animal Center of China Medical University.The pregnant rats were randomly divided into IUGR group and control group according to the order of conception.The control group was fed with normal diet,while the IUGR group was fed with low-protein diet.The offspring were named IUGR group and control group respectively.The expressions of positive cells of Glu,GluR1,GABA and GABAA in cerebral cortex of normal offspring and IUGR offspring were observed by immunohistochemistry.Results Immunohistochemical staining showed that the glutamate positive field of vision in IUGR group was more than that in control group (x2 =82.69,P ＜ 0.05).The glutamate receptor GluR1 positive field of vision in IUGR group was more than that in control group (x2 =76.91,P ＜0.05),while the gamma-aminobutyric acid and its receptors in IUGR group were lower than those in control group (x2 =91.51,x2 =24.05,respectively).The difference was statistically significant (P ＜ 0.05).Conclusion Intrauterine growth retardation can increase the expression of excitatory amino acids and receptors while decrease the expression of inhibitory amino acids and their receptors.Increased expression of excitatory amino acids and receptors and decreased expression of inhibitory amino acids and their receptors may be one of the mechanisms of epilepsy in patients with intrauterine growth retardation.