Szerb J C, Ross T E, Gurevich L
J Neurochem. 1981 Nov;37(5):1186-92. doi: 10.1111/j.1471-4159.1981.tb04669.x.
To establish compartments involved in depolarization-induced release of gamma-aminobutyric acid (GABA) in rat brain slices, the amount of exogenous labeled and endogenous GABA released and retained was followed during 48 min exposure to 50 mM-K+ or to 50 microM-veratridine. Endogenous GABA was measured with high performance liquid chromatography. The presence of 10 microM-aminooxyacetic acid throughout prevented both the metabolism of GABA and the formation of endogenous GABA due to depolarization. During superfusion with 50 mM-K+ and 2.6 nM-Ca2+ the efflux of labeled and endogenous GABA after an initial large increase declined to 10% of the highest value with constant and identical rates. Kinetic analysis of efflux showed that 10% of endogenous and 25% of labeled GABA present is available for release by high K+ and Ca2+. In the absence of Ca2+, release by high K+ of both labeled and endogenous GABA was nearly suppressed. Veratridine, unlike high K+, caused an efflux which declined with an initial fast and late very slow phase. The slow efflux by veratridine was doubled in the absence of Ca2+. Exposure to veratridine in the absence of Ca2+ during 120 min released nearly 70% of labeled and endogenous GABA present. Results suggest that only about 0.25 mumol . g-1 endogenous GABA is the source of physiological Ca2+-dependent release, while much of the remaining GABA present is released only under unphysiological conditions.
为确定大鼠脑片中参与去极化诱导的γ-氨基丁酸（GABA）释放的区室，在暴露于50 mM - K⁺或50 μM藜芦定的48分钟内，跟踪外源性标记GABA和内源性GABA的释放量及留存量。内源性GABA通过高效液相色谱法测定。全程存在10 μM氨氧基乙酸可防止GABA的代谢以及去极化导致的内源性GABA的形成。在用50 mM - K⁺和2.6 nM - Ca²⁺进行灌流期间，标记GABA和内源性GABA的流出量在最初大幅增加后下降至最高值的10%，且速率恒定且相同。流出动力学分析表明，存在的内源性GABA的10%和标记GABA的25%可通过高钾和钙释放。在无钙的情况下，高钾对标记GABA和内源性GABA的释放几乎被抑制。与高钾不同，藜芦定引起的流出量最初快速下降，后期非常缓慢。在无钙的情况下，藜芦定引起的缓慢流出量增加了一倍。在无钙的情况下暴露于藜芦定120分钟，释放了存在的标记GABA和内源性GABA的近70%。结果表明，仅约0.25 μmol·g⁻¹的内源性GABA是生理性钙依赖性释放的来源，而其余大部分存在的GABA仅在非生理性条件下释放。
