Derouiche A
Institute of Anatomy, J. W. Goethe-University, Frankfurt/M., Germany.
Vision Res. 1996 Dec;36(24):3875-8. doi: 10.1016/s0042-6989(96)00140-x.
It is not known how glutamate released synaptically in the outer plexiform layer of the retina is inactivated. Since there is no extracellular enzymatic degradation, glutamate released from photoreceptors is taken up intracellularly by at least one of the three transporters known, and metabolized by a glutamate degrading enzyme. In order to elucidate which of the transporters and enzymes are involved in this process, immuno-electron microscopy was carried out on retinal sections of adult albino rats, applying antiserum against either glutamine synthetase (GS) or L-glutamate-L-aspartate transporter (GLAST). Both stainings revealed immunoreactivity in Müller cells and particularly in their processes tightly ensheathing rod photoreceptor terminals. Thus, although this remains to be tested functionally, transmitter uptake and subsequent degradation at photoreceptor terminals might be preferentially controlled by GLAST and GS expressed in the fine Müller cell processes.
目前尚不清楚视网膜外丛状层中通过突触释放的谷氨酸是如何失活的。由于不存在细胞外酶促降解,光感受器释放的谷氨酸通过已知的三种转运体中的至少一种被细胞内摄取,并由谷氨酸降解酶代谢。为了阐明哪些转运体和酶参与了这一过程,我们对成年白化大鼠的视网膜切片进行了免疫电子显微镜检查,使用了针对谷氨酰胺合成酶(GS)或L-谷氨酸-L-天冬氨酸转运体(GLAST)的抗血清。两种染色均显示在Müller细胞中,特别是在其紧密包裹视杆光感受器终末的突起中有免疫反应性。因此,尽管这仍有待功能测试,但光感受器终末处的递质摄取及随后的降解可能主要由Müller细胞细突起中表达的GLAST和GS控制。