摘要
目的:观察大鼠海马神经元模拟缺血时谷氨酸诱发电流的改变,探讨脑缺血神经元损伤的兴奋毒性机制,为中枢神经损伤的康复提供理论依据。方法:以原代培养的大鼠海马神经元为标本,采用全细胞膜片钳方法观察原代培养大鼠海马神经元模拟缺血时谷氨酸诱发电流改变。结果:当钳制电压为-60mV时,100μmol/L的N-甲基-D-天门冬氨酸(NMDA)、α-氨基-3羟基-5-甲基-4-异恶唑丙酸(AMPA)分别诱发一内向电流(INMDA,IAMPA),模拟缺血处理后的神经元INMDA、IAMPA明显增大。结论:升高的兴奋性氨基酸激活突触后膜的兴奋性氨基酸受体后引起神经细胞损伤。
AIM:To observe the change of simulated is chemia on glutamate-induced currents,and to explore the mechani sm of exitotoxicity of neurons-inju red in cerebral ischemia so as to provide th eory of of central injury of nerve reh a-bilitation.METHODS:The simulated ischemia on glutamate-induced currents in hippocampal primary-curtured neur ons from rats were observed by whole-cell clamp technique.RESULTS:Glutamate,N-methyl-D-aspartate(NMDA)and Alpha-amino-3-hydroxy-5-methylisoxazole-4-pro prionic acid(AMPA)induced an inward current at a holding potential(Vh)of-60mV by whole-cell patch clamp recording,and the conductances of N MDA,AMPA currents in simulated is-chemia neurons were increased over t hose of control neurons.
出处
《中国临床康复》
CSCD
2003年第28期3824-3825,共2页
Chinese Journal of Clinical Rehabilitation
关键词
大鼠
海马神经元
脑缺血
谷氨酸
电流改变
电生理学
Excitatory amino acids receptor of i ncreasing excitatory amino acids synapse posterior induce nerve cell injury.
