Djamgoz M B
Department of Pure and Applied Biology, Neurobiology Group, Imperial College, London SW7 2BB, England.
Neurochem Int. 1988;13(4):439-48. doi: 10.1016/0197-0186(88)90072-1.
The effect of (l-)glutamate on extracellular K(+) activity of the isolated retina of the cyprinid fish, roach, was investigated using double-barrelled K(+)-sensitive micro-electrodes. Application of ?M-mM glutamate to the retina as a "puff" from an atomizer induced a transient rise in extracellular K(+) activity, which was maximal 50-100 ?m below the photoreceptor surface. The effect was concentration-dependent, but not related to the state of light adaptation of the retina. In the presence of dinitrophenol or ouabain, the glutamate-induced increase in extracellular K(+) activity was maintained. The following conclusions are made. (1) The most likely cellular origin(s) of the glutamate-induced rise in extracellular K(+) activity are the photoreceptors and/or the Muller (glial) cells. (2) The mechanism responsible for returning the extracellular K(+) activity to normal depends strongly on metabolic, Na(+), K(+) pump activity. (3) The effect parallels the action of endogenous glutamate, and may be important for modulation of neurotransmission in the intact retina.
使用双管钾离子敏感微电极，研究了（左旋）谷氨酸对鲤科鱼类拟鲤离体视网膜细胞外钾离子活性的影响。用雾化器将微摩尔至毫摩尔浓度的谷氨酸“喷注”到视网膜上，可引起细胞外钾离子活性短暂升高，在光感受器表面下方50 - 100微米处达到最大值。该效应呈浓度依赖性，但与视网膜的光适应状态无关。在存在二硝基苯酚或哇巴因的情况下，谷氨酸诱导的细胞外钾离子活性增加得以维持。得出以下结论：（1）谷氨酸诱导的细胞外钾离子活性升高最可能的细胞来源是光感受器和/或米勒（神经胶质）细胞。（2）使细胞外钾离子活性恢复正常的机制强烈依赖于代谢、钠钾泵活性。（3）该效应与内源性谷氨酸的作用相似，可能对完整视网膜中神经传递的调节很重要。
