Urazaev A Kh, Gafurov B Sh, Grossfeld R M, Fletcher P L, Lieberman E M
Department of Physiology, East Carolina University School of Medicine, Greenville, NC 27858b, USA.
Ross Fiziol Zh Im I M Sechenova. 2001 Apr;87(4):476-91.
Studies of crayfish Medial Giant nerve Fiber suggested that glutamate (GLU) released from the axon during action potential generation initiates metabolic and electrical responses of periaxonal glia. This investigation sought to elucidate the mechanism of GLU appearance extracellularly following axon stimulation. Axoplasm and periaxonal glial sheath from nerve fibers incubated with radiolabelled L-GLU contained radiolabeled GLU, glutamine (GLN), GABA, aspartate (ASP), and NAAG. Total radiolabel release was not altered by electrical stimulation of nerve cord loaded with [14C]-GLU by bath application or loaded with [14C]-GLU, [3H]-D-ASP, or [3H]-NAAG by axonal injection. However, radioactivity distribution among GLU and its metabolic products in the superfusate was changed, with NAAG accounting for the largest fraction. In axons incubated with radiolabeled GLU, the stimulated increase in radioactive NAAG in the superfusate coincided with the virtual clearance of radioactive NAAG from the axon. The increase in [3H]-GLU in the superfusion solution that was seen upon stimulation of nerve bathloaded with [3H]-NAAG was reduced when beta-NAAG, a competitive NAALADase inhibitor, was present. Together, these results suggest that some GLU is metabolized to NAAG in the giant axon and its periaxonal glia and that, upon stimulation, NAAG is released and converted to GLU by NAALADase. A quisqualate-, beta-NAAG-sensitive NAALADase activity was detected in nerve cord homogenates. Stimulation or NAAG administration in the presence of NAALADase inhibitor caused a transient hyperpolarization of the periaxonal glia comparable to that produced by L-GLU. The results implicate N-acetylaspartylglutamate (NAAG) and GLU as potential mediators. of the axon-glia interactions.
对小龙虾内侧巨神经纤维的研究表明，动作电位产生期间从轴突释放的谷氨酸（GLU）引发轴周神经胶质细胞的代谢和电反应。本研究旨在阐明轴突刺激后细胞外GLU出现的机制。用放射性标记的L-GLU孵育的神经纤维的轴浆和轴周神经胶质鞘含有放射性标记的GLU、谷氨酰胺（GLN）、GABA、天冬氨酸（ASP）和NAAG。通过浴槽给药加载[14C]-GLU或通过轴突注射加载[14C]-GLU、[3H]-D-ASP或[3H]-NAAG对神经索进行电刺激，总放射性标记释放未改变。然而，超滤液中GLU及其代谢产物之间的放射性分布发生了变化，NAAG占最大比例。在用放射性标记的GLU孵育的轴突中，超滤液中放射性NAAG的刺激增加与轴突中放射性NAAG的几乎清除相吻合。当存在竞争性NAALADase抑制剂β-NAAG时，用[3H]-NAAG加载神经浴刺激后超滤液中[3H]-GLU的增加减少。总之，这些结果表明，一些GLU在巨轴突及其轴周神经胶质细胞中代谢为NAAG，并且在刺激时，NAAG被释放并被NAALADase转化为GLU。在神经索匀浆中检测到对quisqualate、β-NAAG敏感的NAALADase活性。在NAALADase抑制剂存在下进行刺激或给予NAAG会导致轴周神经胶质细胞短暂超极化，类似于L-GLU产生的超极化。结果表明N-乙酰天冬氨酰谷氨酸（NAAG）和GLU是轴突-神经胶质细胞相互作用的潜在介质。
