title: Effects of DIDS on the chick retinal pigment epithelium. II. Mechanism of the light peak and other responses originating at the basal membrane.
abstract: 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)
authors.affiliation: Department of Physiology, University of California, San Francisco 94143.
authors.forename: R P
authors.initials: RP
authors.lastname: Gallemore
authors.forename: R H
authors.initials: RH
authors.lastname: Steinberg
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000031:analogs & derivatives / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D000838:Anions / Q000037:antagonists & inhibitors / Q000378:metabolism; D001386:Azides / Q000494:pharmacology; D001696:Biomechanical Phenomena; D002645:Chickens; D002829:Choroid / Q000187:drug effects / Q000502:physiology; D004594:Electrophysiology; D004596:Electroretinography; D066298:In Vitro Techniques; D008027:Light; D008566:Membranes / Q000187:drug effects / Q000502:physiology; D009994:Osmolar Concentration; D010857:Pigment Epithelium of Eye / Q000187:drug effects / Q000502:physiology*; D012160:Retina / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D019810:Sodium Azide; D013267:Stilbenes / Q000494:pharmacology*
chemical_list: D000838:Anions; D001386:Azides; D013267:Stilbenes; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D019810:Sodium Azide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid