Maruiwa F, Nao-i N, Nakazaki S, Sawada A
Department of Ophthalmology, Miyazaki Medical College, Japan.
Curr Eye Res. 1995 Aug;14(8):685-91. doi: 10.3109/02713689508998496.
We examined the effects of adenosine, a putative mediator of neuroprotection during cerebral ischemia, on the electrophysiological characteristics of retina-retinal pigment epithelium-choroid preparations obtained from 1-7 day-old chick and maintained in vitro. Our experiments produced the following results. First, superfusion of the retinal surface with adenosine (0.1 mM) increased the trans-tissue potential. The trans-epithelial (but not the trans-retinal) potential was also increased to the same magnitude with a time-course similar to that of the trans-tissue potential. Second, adenosine produced a depolarization of the epithelial basal plasma membrane with a concomitant decrease in its basal membrane resistance. Third, the trans-epithelial (but not the trans-retinal) c-wave in response to a light stimulus was augmented by adenosine. Adenosine reduced the hyperpolarization of the epithelial basal membrane, but had no effect on the extracellular concentration of K+ in the subretinal region. Fourth, the light-peak that was elicited with a 300 s light stimulus was also depressed by adenosine. Fifth, when 4,4'-diisothiocy anostilbene-2,2'-disulfonate (DIDS), a relatively selective inhibitor of Cl- channels, was perfused at 50 microM on the choroidal surface, adenosine-induced increases in the trans-tissue potential and the c-wave were both abolished. These results suggest that adenosine increased the Cl- conductance of the basal plasma membrane of the retinal pigment epithelium and thereby augmented the standing potential as well as the light-elicited membrane potentials of the retinal pigment epithelium, which seems to be involved in the pathophysiology of retinal ischemia.
我们研究了腺苷（一种在脑缺血期间可能起神经保护作用的介质）对从1至7日龄雏鸡获取并在体外维持的视网膜-视网膜色素上皮-脉络膜标本电生理特性的影响。我们的实验得出了以下结果。首先，用腺苷（0.1 mM）对视网膜表面进行灌流可增加跨组织电位。跨上皮（而非跨视网膜）电位也以与跨组织电位相似的时间进程增加到相同幅度。其次，腺苷使上皮基底质膜去极化，同时其基底膜电阻降低。第三，腺苷增强了对光刺激的跨上皮（而非跨视网膜）c波。腺苷减少了上皮基底膜的超极化，但对视网膜下区域的细胞外钾离子浓度没有影响。第四，腺苷也抑制了由300秒光刺激引发的光峰。第五，当在脉络膜表面以50 microM灌流相对选择性的Cl-通道抑制剂4,4'-二异硫氰基芪-2,2'-二磺酸盐（DIDS）时，腺苷诱导的跨组织电位增加和c波均被消除。这些结果表明，腺苷增加了视网膜色素上皮基底质膜的Cl-电导，从而增强了视网膜色素上皮的静息电位以及光诱发的膜电位，这似乎与视网膜缺血的病理生理学有关。
