Bigelow J C, Brown D S, Wightman R M
J Neurochem. 1984 Feb;42(2):412-9. doi: 10.1111/j.1471-4159.1984.tb02693.x.
Gamma-aminobutyric acid (GABA) was found to induce the release of ascorbic acid from rat striatal homogenates and minces. This release was studied with the use of a rapid superfusion system with an on-line amperometric detector that monitors for the presence of easily oxidized substances (i.e., ascorbate, 3,4-dihydroxyphenylethylamine). The release was found to be calcium-independent and depolarization-dependent. This releasable pool of ascorbate could be replenished through nonstereospecific uptake. The releasing action of GABA was mimicked by the GABA agonist, muscimol, and was completely inhibited by the GABA antagonist, picrotoxin. The structural analogues of GABA, beta-alanine and gamma-hydroxybutyric acid, had no effect. These data indicate that ascorbate release is GABA-receptor mediated and synaptically localized.
发现γ-氨基丁酸(GABA)可诱导大鼠纹状体匀浆和切碎组织释放抗坏血酸。使用带有在线安培检测器的快速灌注系统对这种释放进行了研究,该检测器可监测易氧化物质(即抗坏血酸盐、3,4-二羟基苯乙胺)的存在。发现这种释放与钙无关,而与去极化有关。这种可释放的抗坏血酸池可通过非立体特异性摄取来补充。GABA激动剂蝇蕈醇模拟了GABA的释放作用,而GABA拮抗剂印防己毒素则完全抑制了这种作用。GABA的结构类似物β-丙氨酸和γ-羟基丁酸没有作用。这些数据表明抗坏血酸的释放是由GABA受体介导的,且定位于突触部位。