Herrero I, Miras-Portugal M T, Sánchez-Prieto J
Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, Madrid, Spain.
J Neurochem. 1991 Aug;57(2):718-21. doi: 10.1111/j.1471-4159.1991.tb03805.x.
The action of arachidonic acid on glutamate release in rat cerebrocortical synaptosomes was investigated. The Ca(2+)-dependent release of glutamate evoked by 4-aminopyridine (4-AP) was inhibited by arachidonic acid (0.5-10 microM), but the KCl-evoked release was not modified. The Ca(2+)-independent release of glutamate was insensitive to low concentrations of arachidonic acid, but higher concentrations of this free fatty acid (30 microM) induced a slow efflux of cytoplasmic glutamate. The decrease in the Ca(2+)-dependent release of glutamate by arachidonic acid was consistent with a reduction in both the depolarization and the subsequent rise in the cytoplasmic free Ca2+ concentration induced by 4-AP in the nerve terminal. The inhibitory action by arachidonic acid observed in glutamate release was reversed in the presence of the K(+)-channel blocker tetraethylammonium.
研究了花生四烯酸对大鼠大脑皮质突触体中谷氨酸释放的作用。花生四烯酸（0.5 - 10微摩尔）抑制了4 - 氨基吡啶（4 - AP）诱发的依赖于钙的谷氨酸释放，但对氯化钾诱发的释放没有影响。不依赖于钙的谷氨酸释放对低浓度花生四烯酸不敏感，但较高浓度的这种游离脂肪酸（30微摩尔）会诱导细胞质中谷氨酸的缓慢外流。花生四烯酸使依赖于钙的谷氨酸释放减少，这与神经末梢中4 - AP诱导的去极化以及随后细胞质游离钙离子浓度的升高降低是一致的。在钾离子通道阻滞剂四乙铵存在的情况下，观察到的花生四烯酸对谷氨酸释放的抑制作用被逆转。
