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Effects of adenosine on chick retinal pigment epithelium: membrane potentials and light-evoked responses
F Maruiwa1, N Nao-i, S Nakazaki
1Department of Ophthalmology, Miyazaki Medical College, Japan.
Insights
Adenosine enhances retinal pigment epithelium function by increasing chloride channel activity, potentially aiding neuroprotection during ischemia. This study investigates adenosine
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Physiology
Background:
- Cerebral ischemia can lead to retinal damage.
- Adenosine is a potential neuroprotective agent.
- Retinal pigment epithelium (RPE) plays a crucial role in retinal function.
Purpose of the Study:
- To investigate the electrophysiological effects of adenosine on the retina-retinal pigment epithelium-choroid complex.
- To elucidate the role of adenosine in RPE function and its potential relevance to retinal ischemia.
Main Methods:
- In vitro electrophysiological recordings from chick retina-retinal pigment epithelium-choroid preparations.
- Superfusion with adenosine and DIDS (a chloride channel inhibitor).
- Measurement of trans-tissue, trans-epithelial, and trans-retinal potentials, as well as c-wave and light-peak responses.
Main Results:
- Adenosine increased trans-tissue and trans-epithelial potentials.
- Adenosine caused RPE basal plasma membrane depolarization and decreased resistance.
- Adenosine augmented light-elicited c-waves but depressed light-peaks; DIDS abolished these effects.
Conclusions:
- Adenosine increases chloride conductance in the RPE basal plasma membrane.
- This action augments RPE standing and light-elicited potentials.
- Adenosine's effects on RPE may be involved in the pathophysiology of retinal ischemia.
Abstract:
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.