Harada T, Harada C, Watanabe M, Inoue Y, Sakagawa T, Nakayama N, Sasaki S, Okuyama S, Watase K, Wada K, Tanaka K
Department of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502, Japan.
Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4663-6. doi: 10.1073/pnas.95.8.4663.
In the retina, the glutamate transporter GLAST is expressed in Müller cells, whereas the glutamate transporter GLT-1 is found only in cones and various types of bipolar cells. To investigate the functional role of this differential distribution of glutamate transporters, we have analyzed GLAST and GLT-1 mutant mice. In GLAST-deficient mice, the electroretinogram b-wave and oscillatory potentials are reduced and retinal damage after ischemia is exacerbated, whereas GLT-1-deficient mice show almost normal electroretinograms and mild increased retinal damage after ischemia. These results demonstrate that GLAST is required for normal signal transmission between photoreceptors and bipolar cells and that both GLAST and GLT-1 play a neuroprotective role during ischemia in the retina.
在视网膜中，谷氨酸转运体GLAST在穆勒细胞中表达，而谷氨酸转运体GLT-1仅存在于视锥细胞和各种类型的双极细胞中。为了研究谷氨酸转运体这种差异分布的功能作用，我们分析了GLAST和GLT-1突变小鼠。在GLAST缺陷小鼠中，视网膜电图b波和振荡电位降低，缺血后视网膜损伤加剧，而GLT-1缺陷小鼠的视网膜电图几乎正常，缺血后视网膜损伤轻度增加。这些结果表明，GLAST是光感受器和双极细胞之间正常信号传递所必需的，并且GLAST和GLT-1在视网膜缺血期间均发挥神经保护作用。
