Mori S, Miller W H, Tomita T
Jpn J Physiol. 1976;26(2):219-33. doi: 10.2170/jjphysiol.26.219.
By means of K+ microelectrodes, K+ potentials and [K+] were studied in frog retinas conditioned for SD by CL--free Ringer's. A marked increase in [K+]o was observed during SD, the increase being maximal in the inner plexiform layer (up to 50 mM or more) and subsiding towards the distal retina. The extracellular K+ potential change during SD and also the graded K+ potential changes produced locally by iontophoretic injection of SD-stimulant chemicals resembled the membrane potential changes in Müller cells under the same conditions, suggesting that the Müller cells act as K+ electrodes. In retinas conditioned by Cl--free Ringer's Müller cells were swollen. This allowed intracellular recording with K+ electrodes in Müller cells to reveal that upon SD the Müller cells immediately start to cleanse the extracellular space of excess K+ which is probably a product of pathologically enhanced synaptic activity in the inner plexiform layer. The mechanism of SDP, the field potential change associated with SD, is discussed from a proposed model.
通过钾离子微电极,在无氯离子林格氏液条件下对经历睡眠剥夺(SD)的青蛙视网膜中的钾离子电位和[钾离子]进行了研究。在睡眠剥夺期间观察到[钾离子]o显著增加,这种增加在内网状层最大(高达50 mM或更高),并向视网膜远端逐渐减弱。睡眠剥夺期间细胞外钾离子电位的变化以及通过离子电渗注入睡眠剥夺刺激化学物质局部产生的分级钾离子电位变化,类似于相同条件下米勒细胞的膜电位变化,这表明米勒细胞起到了钾离子电极的作用。在无氯离子林格氏液条件下处理的视网膜中,米勒细胞肿胀。这使得能够用钾离子电极在米勒细胞中进行细胞内记录,从而揭示在睡眠剥夺时,米勒细胞立即开始清除细胞外空间中多余的钾离子,这可能是内网状层病理性增强的突触活动的产物。从一个提出的模型讨论了与睡眠剥夺相关的场电位变化——睡眠剥夺电位(SDP)的机制。