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Investigative Ophthalmology & Visual Science, Vol 34, 2009-2017, Copyright © 1993 by Association for Research in Vision and Ophthalmology
ARTICLES AND REPORTS |
F Yamamoto and Y Honda
Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
PURPOSE. Effects of intravenous iodoacetate (a glycolysis inhibitor) and iodate (a metabolism inhibitor selective to retinal pigment epithelium) on light-evoked alkalinizations and hypoxia-induced acidifications were studied in the dark-adapted cat retina, in vivo, to learn about pH regulation. METHODS. pH was recorded in the extracellular space surrounding rod photoreceptors with double- barrelled H(+)-selective microelectrodes. RESULTS. Intravenous infusion of 5 mg/kg iodoacetate-induced alkalinizations in the outer nuclear layer and suppressed both light-evoked and hypoxia-induced pH responses immediately. Iodate injection (30 mg/kg) produced acidifications in the subretinal space and affected light-evoked alkalinizations gradually but not hypoxia-induced acidifications. CONCLUSIONS. These results suggest that rods glycolysis plays an important role in both light- evoked and hypoxia-induced pH responses. And the retinal pigment epithelium may have little concern with light-evoked alkalinizations except that it plays an important role in regenerating the rhodopsin to be needed for the light responses of photoreceptors. Furthermore, the finding of the intravenous-iodoacetate-induced alkalinization in the outer nuclear layer supports that acid production by rods in the dark is originated from glycolysis to support the dark current. The iodate- induced acidification in the subretinal space indicators that the retinal pigment epithelium might actively transport acids from the subretinal space to the choroid.
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