Szerb J C, Issekutz B
Brain Res. 1987 Apr 28;410(1):116-20. doi: 10.1016/s0006-8993(87)80030-6.
Fluoroacetate is known to be taken up selectively by glia, where after forming fluorocitrate, it inhibits the tricarboxylic acid cycle. Since uptake into glia has a major role in the inactivation of synaptically released glutamate, the effect of fluoroacetate on the overflow of glutamate evoked by electrical field stimulation in slices of rat hippocampus was investigated. In agreement with previous reports, 1 mM fluoroacetate reduced the release and content of glutamine, but increased only slightly the overflow of glutamate induced by stimulation. If, however, 0.5 mM glutamine was added to the superfusion fluid, fluoroacetate nearly tripled the overflow of glutamate evoked by electrical field stimulation. The large glutamate overflow due to field stimulation in the presence of fluoroacetate was fully Ca2+ -dependent. Results confirm the major role of glia in the inactivation of glutamate. The absence of such an uptake may contribute to the in vivo convulsive effect of fluoroacetate.
已知氟乙酸盐可被神经胶质细胞选择性摄取，在形成氟柠檬酸后，它会抑制三羧酸循环。由于摄取到神经胶质细胞中在使突触释放的谷氨酸失活方面起主要作用，因此研究了氟乙酸盐对大鼠海马切片中电场刺激诱发的谷氨酸溢出的影响。与先前的报道一致，1 mM氟乙酸盐降低了谷氨酰胺的释放和含量，但仅略微增加了刺激诱导的谷氨酸溢出。然而，如果在灌流液中添加0.5 mM谷氨酰胺，氟乙酸盐会使电场刺激诱发的谷氨酸溢出增加近两倍。在氟乙酸盐存在下，电场刺激导致的大量谷氨酸溢出完全依赖于Ca2+。结果证实了神经胶质细胞在谷氨酸失活中的主要作用。缺乏这种摄取可能导致氟乙酸盐在体内的惊厥作用。
