Na^+,K^+-ATP酶参与大鼠皮层神经元NMDA电流的调节

Comprehensive study of N-methyl-D-aspartate current involving Na^+,K^+-ATPase in rat cortical neuron

目的观察Na+,K+-ATP酶是否参与神经元缺氧后兴奋性氨基酸电流的改变及其发生机制。方法利用全细胞脑片膜片钳技术,记录出生12～16 d的SD乳大鼠脑片皮层神经元在正常和缺氧时的NMDA电流,分别观察不同浓度的双氢哇巴因(dihydroouabain,DHO)对此电流的影响。结果无论在正常或缺氧条件下,不同浓度的DHO(10-11～10-3 mol.L-1)和矾酸钠(vanadate)均能浓度依赖性抑制皮层神经元的NMDA电流,然而,孵育不同浓度DHO后引起的NMDA电流密度在低氧时明显大于常氧时。结论提示神经元Na+,K+-ATP酶参与NMDA电流的调节,但低氧时主要由兴奋性氨基酸调节。

Aim To explore under normoxia and hypoxia conditions whether the Na＋,K＋-ATPase was involved in the change of the excitatory amino acid current in rat cortical neuron and its mechanism.Methods The whole-cell mode was used to examine NMDA current in rat brain slices by the patch clamp systems with infrared differential interference contrast（IR-DIC） optics and to observe the effects of different con-centrations of dihydroouabain（DHO） on NMDA current.Results Under either normoxia or hypoxia conditions,DHO and vanadate decreased the NMDA current in a concentration-dependent manner.However,NMDA current densities decreased by different concentrations of DHO were much larger under hypoxia than those under normoxia.Conclusion The regulation of NMDA current of cortical neuron after hypoxia may depend mainly on the release of excitatory amino acid,not the function of the Na＋,K＋-ATPase.