Hanitzsch R
Carl-Ludwig-Institute of Physiology, University Leipzig, Germany.
Doc Ophthalmol. 1993;84(3):267-78. doi: 10.1007/BF01203659.
Light-induced extracellular potassium changes were measured in the isolated rabbit retina superfused by a plasma saline mixture and compared with the electroretinogram. When the transmission to second-order neurons was blocked by aspartate and glutamate or by Mg2+, the electroretinogram consisted of the receptor potential and the cornea-negative slow PIII. Since the onset of PIII could then be seen to precede the decrease in extracellular potassium concentration ([K+]0) around photoreceptors, the [K+]0 decrease could not be the cause of the onset of slow PIII. A possible source for the initial phase of slow PIII could be the electrogenic Na+/bicarbonate transporter mechanism of glial cells. Slow PIII depended highly on the extracellular sodium concentration, and it was larger in solutions buffered with bicarbonate than with HEPES, while the [K+]0 decrease around receptors was unchanged.
在由血浆盐水混合物灌注的离体兔视网膜中测量光诱导的细胞外钾变化,并与视网膜电图进行比较。当通过天冬氨酸和谷氨酸或Mg2+阻断向二级神经元的传递时,视网膜电图由感受器电位和角膜负向慢PIII组成。由于此时可以看到PIII的起始先于光感受器周围细胞外钾浓度([K+]0)的降低,因此[K+]0的降低不可能是慢PIII起始的原因。慢PIII初始阶段的一个可能来源可能是神经胶质细胞的电致Na+/碳酸氢盐转运机制。慢PIII高度依赖于细胞外钠浓度,并且在用碳酸氢盐缓冲的溶液中比用HEPES缓冲的溶液中更大,而感受器周围的[K+]0降低没有变化。