Huang R, Shuaib A, Hertz L
Department of Pharmacology, University of Saskatchewan, Saskatoon, Canada.
Brain Res. 1993 Aug 6;618(2):346-51. doi: 10.1016/0006-8993(93)91289-5.
During brain ischemia in vivo the extracellular concentration of the excitotoxic amino acid, glutamate, increases. This increase could be caused either by an enhanced formation rate of glutamate (from glutamine) or by an impaired re-uptake (or both). This re-uptake occurs to a large extent in astrocytes. In the present study we have determined glutamate uptake and the ability of the cells to maintain their glutamate content during exposure to anoxia, substrate deprivation and combined substrate deprivation and anoxia ('simulated ischemia') for a duration of up to 4 h. Isolated anoxia had no significant effect, whereas both substrate deprivation alone and 'simulated ischemia' reduced glutamate uptake and glutamate content by one-half after 2 h. Under hypothermic conditions (incubation at 32 degrees C), which in in vivo experiments exerts some protection against ischemic cell death in neurons, ischemia of intermediate duration (2 h) decreased glutamate uptake and glutamate content to a less extent than at 37 degrees C. Hypothermia did not have a similar effect during exposure to isolated substrate deprivation.
在体内脑缺血期间，兴奋性毒性氨基酸谷氨酸的细胞外浓度会升高。这种升高可能是由于谷氨酸（从谷氨酰胺）生成速率增强，或者是再摄取受损（或两者皆有）所致。这种再摄取在很大程度上发生在星形胶质细胞中。在本研究中，我们测定了谷氨酸摄取以及细胞在暴露于缺氧、底物剥夺以及底物剥夺与缺氧联合（“模拟缺血”）长达4小时期间维持其谷氨酸含量的能力。单纯缺氧没有显著影响，而单独的底物剥夺和“模拟缺血”在2小时后使谷氨酸摄取和谷氨酸含量降低了一半。在低温条件下（32℃孵育），在体内实验中这种条件对神经元缺血性细胞死亡有一定保护作用，中等时长（2小时）的缺血比在37℃时对谷氨酸摄取和谷氨酸含量的降低程度要小。在单纯底物剥夺暴露期间，低温没有类似作用。
