Tanaka K
Laboratory for Neural Networks, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.
Brain Res Mol Brain Res. 1994 Jan;21(1-2):167-70. doi: 10.1016/0169-328x(94)90390-5.
Pharmacological properties of a cDNA clone encoding a high affinity, Na(+)-dependent L-glutamate transporter (GluT-1) were examined using Xenopus oocytes. L-[3H]glutamate transport was inhibited by the putative endogenous substrates L-aspartate (Ki = 65 microM) and L-glutamate (Ki = 70 microM). L-Homocysteate did not significantly inhibit high-affinity glutamate transport (Ki = 2.7 mM). Of the previously identified uptake inhibitors, DL-threo-beta-hydroxyaspartate (Ki = 65 microM), L-cysteine sulfinate (Ki = 80 microM), beta-glutamate (Ki = 475 microM) and L-aspartate-beta-hydroxamate (Ki = 950 microM) inhibited L-glutamate uptake. The other L-glutamate uptake blockers examined, including dihydrokainate, L-alpha-aminoadipate and SITS, weakly inhibited uptake of L-glutamate with Ki values in excess of 1 mM. These features of the inhibitor sensitivities of GluT-1 transport show that GluT-1 is less sensitive to these agents than previously characterized glutamate transporters in rat brain, suggesting that GluT-1 is a novel glutamate transporter with a unique pharmacologic profile.
利用非洲爪蟾卵母细胞研究了编码高亲和力、钠离子依赖性L-谷氨酸转运体（GluT-1）的cDNA克隆的药理学特性。L-[3H]谷氨酸转运受到假定的内源性底物L-天冬氨酸（Ki = 65微摩尔）和L-谷氨酸（Ki = 70微摩尔）的抑制。L-高半胱氨酸对高亲和力谷氨酸转运没有显著抑制作用（Ki = 2.7毫摩尔）。在先前鉴定的摄取抑制剂中，DL-苏式-β-羟基天冬氨酸（Ki = 65微摩尔）、L-半胱氨酸亚磺酸盐（Ki = 80微摩尔）、β-谷氨酸（Ki = 475微摩尔）和L-天冬氨酸-β-异羟肟酸（Ki = 950微摩尔）抑制L-谷氨酸摄取。所检测的其他L-谷氨酸摄取阻滞剂，包括二氢海人藻酸、L-α-氨基己二酸和SITS，对L-谷氨酸摄取的抑制作用较弱，Ki值超过1毫摩尔。GluT-1转运抑制剂敏感性的这些特征表明，GluT-1对这些药物的敏感性低于大鼠脑中先前表征的谷氨酸转运体，提示GluT-1是一种具有独特药理学特征的新型谷氨酸转运体。
