Butcher S P, Sandberg M, Hagberg H, Hamberger A
J Neurochem. 1987 Mar;48(3):722-8. doi: 10.1111/j.1471-4159.1987.tb05576.x.
The effect of severe insulin-induced hypoglycemia on the extracellular levels of endogenous amino acids in the rat striatum was examined using the brain microdialysis technique. A characteristic pattern of alterations consisting of a 9-12-fold increase in aspartate (Asp), and more moderate increases in glutamate (Glu), taurine (Tau), and gamma-aminobutyric acid (GABA), was noted following cessation of electroencephalographic activity (isoelectricity). Glutamine (Gln) levels were reduced both during and after the isoelectric period and there was a delayed increase in extracellular phosphoethanolamine (PEA) content. The effects of decortication and excitotoxin lesions on the severe hypoglycemia-evoked efflux of endogenous amino acids in the striatum were also examined. Decortication reduced the release of Glu and Asp both 1 week and 1 month post-lesion. The efflux of other neuroactive amino acids was not affected significantly. In contrast, GABA, Tau, and PEA efflux was attenuated in kainate-lesioned striata. Glu and Asp release was also reduced under these conditions, and a smaller decrease in extracellular Gln was noted. These data suggest that GABA, Glu, and Asp are released primarily from their transmitter pools during severe hypoglycemia. The releasable pools of Tau and PEA appear to be located in kainate-sensitive striatal neurons. The significance of these results is discussed with regard to the excitotoxic theory of hypoglycemic cell death.
采用脑微透析技术研究了严重胰岛素诱导的低血糖对大鼠纹状体中内源性氨基酸细胞外水平的影响。在脑电图活动停止（等电位）后，观察到一种特征性的变化模式，包括天冬氨酸（Asp）增加9 - 12倍，谷氨酸（Glu）、牛磺酸（Tau）和γ-氨基丁酸（GABA）有更适度的增加。在等电位期间及之后谷氨酰胺（Gln）水平均降低，细胞外磷酸乙醇胺（PEA）含量有延迟增加。还研究了去皮质和兴奋性毒素损伤对纹状体中严重低血糖诱发的内源性氨基酸流出的影响。去皮质在损伤后1周和1个月均降低了Glu和Asp的释放。其他神经活性氨基酸的流出未受到显著影响。相比之下，在海藻酸损伤的纹状体中，GABA、Tau和PEA的流出减弱。在这些条件下，Glu和Asp的释放也减少，细胞外Gln有较小程度的降低。这些数据表明，在严重低血糖期间，GABA、Glu和Asp主要从其递质池中释放。Tau和PEA的可释放池似乎位于对海藻酸敏感的纹状体神经元中。就低血糖细胞死亡的兴奋性毒性理论讨论了这些结果的意义。
