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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Synaptic activation of presynaptic glutamate transporter currents in nerve terminals.
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Synaptic activation of presynaptic glutamate transporter currents in nerve terminals.

机译：神经末梢突触前谷氨酸转运蛋白电流的突触激活。

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Glutamate uptake by high-affinity transporters is responsible for limiting the activation of postsynaptic receptors and maintaining low levels of ambient glutamate. The reuptake process generates membrane currents, which can be activated by synaptically released glutamate in glial cells and some postsynaptic neurons. However, less is known about presynaptic transporter currents because the small size of synaptic boutons precludes direct recordings. Here, we have recorded from two giant nerve terminals: bipolar cell synaptic terminals in goldfish retina and the calyx of Held in rat auditory brainstem. Exocytosis was evoked by brief depolarizations and measured as an increase in membrane capacitance. In isolated bipolar cell terminals, exocytosis was associated with an anion (NO3- or Cl-) current. The current peaked 2.8 msec after the start of the depolarization and decayed with a mean time constant of 8.5 msec. It was inhibited by the nontransportable glutamate transporter antagonist sc-threo-beta-benzyloxyaspartate (TBOA) but was insensitive to the GLT1/EAAT2 subtype-selective antagonist dihydrokainate and was affected by extracellular pH buffering. A TBOA-sensitive anion current was also evoked by application of exogenous glutamate to bipolar cell terminals. The large single-channel conductance, derived from noise analysis, and previous immunolocalization studies suggest that synaptically released glutamate activates EAAT5-type transporters in bipolar cell terminals. In contrast, neither exocytosis nor exogenous glutamate evoked a transporter current in the calyx of Held. Glutamate transporter currents with rapid kinetics are therefore identified and characterized in bipolar cell terminals, providing a valuable system for investigating the function and modulation of presynaptic glutamate transporters.
机译：高亲和力转运蛋白对谷氨酸的摄取负责限制突触后受体的活化并维持低水平的环境谷氨酸。再摄取过程产生膜电流，该膜电流可以由胶质细胞和某些突触后神经元中突触释放的谷氨酸激活。但是，关于突触前转运蛋白电流知之甚少，因为突触钮扣的尺寸小，无法进行直接记录。在这里，我们从两个巨大的神经末梢记录下来：金鱼视网膜中的双极细胞突触末梢和大鼠听觉脑干中的花萼。短暂的去极化引起胞吐作用，并测量为膜电容的增加。在孤立的双极细胞末端，胞吐作用与阴离子（NO3-或Cl-）电流相关。去极化开始后，电流峰值达到2.8毫秒，然后衰减，平均时间常数为8.5毫秒。它被不可运输的谷氨酸转运蛋白拮抗剂sc-苏-β-苄氧基天冬氨酸（TBOA）抑制，但对GLT1 / EAAT2亚型选择性拮抗剂dihydrokainate不敏感，并受到细胞外pH缓冲的影响。通过将外源性谷氨酸盐施加到双极细胞末端也引起了TBOA敏感的阴离子电流。从噪声分析和先前的免疫定位研究得出的大单通道电导表明，突触释放的谷氨酸激活了双极细胞末端的EAAT5型转运蛋白。相反，胞吐作用和外源谷氨酸都不在Held的花萼中引起转运蛋白电流。因此，具有快速动力学的谷氨酸转运蛋白电流在双极细胞末端得以鉴定和表征，为研究突触前谷氨酸转运蛋白的功能和调节提供了有价值的系统。

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