Potassium-evoked responses from the retinal pigment epithelium of the toad Bufo marinus.
Changes in the apical and basal membrane potentials and the resultant changes in the transepithelial potential were recorded from the isolated retinal pigment epithelium of the toad Bufo marinus while the potassium concentration superfusing the apical membrane was changed. Lowering apical potassium caused an initial apically-generated hyperpolarization that increased the transepithelial potential which was usually followed by a delayed basally-generated hyperpolarization that decreased the transepithelial potential. Light evoked a similar pattern of apical and basal responses in a preparation of neural retina-retinal pigment epithelium-choroid. The delayed basal hyperpolarization was accompanied by an apparent increase in basal membrane resistance, and was inhibited by adding the anion transport blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid or the metabolic inhibitor dinitrophenol to the solution superfusing the choroidal side of the retinal pigment epithelium (RPE). The results suggest that a change in the chloride equilibrium potential or chloride conductance of the basal membrane mediates the delayed basal response.[1]References
- Potassium-evoked responses from the retinal pigment epithelium of the toad Bufo marinus. Griff, E.R. Exp. Eye Res. (1991) [Pubmed]
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