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Journal of Neuroscience, Vol 9, 1977-1984, Copyright © 1989 by Society for Neuroscience
Effects of DIDS on the chick retinal pigment epithelium. II. Mechanism of the light peak and other responses originating at the basal membrane
RP Gallemore and RH Steinberg
Department of Physiology, University of California, San Francisco 94143.
4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) appears to block a Cl-
conductance in the basal membrane of the chick retinal pigment epithelium
(RPE) (Gallemore and Steinberg, 1989). The present paper describes the
effect of DIDS, as well as effects of anion movement blockade with other
pharmacological agents, on 3 responses that originate as depolarizations of
the RPE basal membrane: the light peak of the DC electroretinogram, the
response to sodium azide, and the response to a small transtissue
hyperosmotic gradient. Intracellular and extracellular potentials, and
measurements of subretinal [K+]o were obtained from an in vitro preparation
of chick retina-RPE-choroid. Choroidal perfusion with each of 4 anion
transport and Cl- channel blockers (DIDS,
4-acetamido-4'-isothiocyanostilbene, phenylanthranylic acid, and
thiocyanate) suppressed the light peak. DIDS, the most potent agent,
abolished the basal membrane light-peak depolarization. Choroidal perfusion
with azide depolarized the basal membrane and decreased its apparent
resistance, Rba, as in cat (Linsenmeier and Steinberg, 1987). The basal
membrane depolarization, recorded extracellularly as an increase in the
transtissue potential (TTP), was blocked by DIDS. Azide also increased RPE
c-wave amplitude, which could be explained by the decrease in Rba, and it
suppressed the light peak. As previously described (Shirao and Steinberg,
1987), a 25 mOsm transtissue hyperosmotic load (retinal side hyperosmotic)
increased the TTP, increased the c-wave and decreased the transtissue
resistance. DIDS suppressed each of these effects. We conclude that the
light peak, the response to azide, and the response to a retinal
hyperosmotic load may each originate as an increase in a basal membrane
anion conductance that may be permeable to chloride.(ABSTRACT TRUNCATED AT
250 WORDS)
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