| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
University of California, School of Optometry, Berkeley 94720, USA.
1. Conventional and ion-selective double-barrelled microelectrodes were used in an in vitro preparation of bovine retinal pigment epithelium (RPE)-choroid to measure the changes in membrane voltage, resistance and intracellular Cl- activity (aCli) produced by small, physiological changes in extracellular potassium concentration ([K+]o). These apical [K+]o changes approximate those produced in the extracellular (subretinal) space between the photoreceptors and the RPE following transitions between light and dark. 2. Changing apical [K+]o from 5 to 2 mM in vitro elicited membrane voltage responses with three distinct phases. The first phase was generated by an apical membrane hyperpolarization, followed by a (delayed) basolateral membrane hyperpolarization (DBMH); the third phase was an apical membrane depolarization. The present experiments focus on the membrane and cellular mechanisms that generate phase 2 of the response, the DBMH. 3. The DBMH was abolished in the presence of apical bumetanide (100 microM); this response was completely restored after bumetanide removal. 4. Reducing apical [K+]o, adding apical bumetanide (500 mM), or removing apical Cl- decreased aCli by 25 +/- 6 (n = 8), 28 +/- 1 (n = 2) and 26 +/- 5 mM (n = 3), respectively; adding 100 microM apical bumetanide decreased aCli by 12 +/- 2 mM (n = 3). Adding apical bumetanide or removing apical bath Cl- hyperpolarized the basolateral membrane and decreased the apparent basolateral membrane conductance (GB). 5. DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid) blocked the RPE basolateral membrane Cl- conductance and inhibited the DBMH and the basolateral membrane hyperpolarization produced by apical bumetanide addition or by removal of apical Cl-o. The present results show that the DBMH is caused by delta[K]o-induced inhibition of the apical membrane Na(+)-K(+)-2Cl- cotransporter; the subsequent decrease in aCli generated a hyperpolarization at the basolateral membrane Cl- channel.
This article has been cited by other articles:
|
|
 |
|
  A. Maminishkis, S. Chen, S. Jalickee, T. Banzon, G. Shi, F. E. Wang, T. Ehalt, J. A. Hammer, and S. S. Miller Confluent monolayers of cultured human fetal retinal pigment epithelium exhibit morphology and physiology of native tissue. Invest. Ophthalmol. Vis. Sci., August 1, 2006; 47(8): 3612 - 3624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Strauss The Retinal Pigment Epithelium in Visual Function Physiol Rev, July 1, 2005; 85(3): 845 - 881. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Qu, R. Fischmeister, and C. Hartzell Mouse Bestrophin-2 Is a Bona fide Cl- Channel: Identification of a Residue Important in Anion Binding and Conduction J. Gen. Physiol., March 29, 2004; 123(4): 327 - 340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.-J. Sheu and S.-N. Wu Mechanism of Inhibitory Actions of Oxidizing Agents on Calcium-Activated Potassium Current in Cultured Pigment Epithelial Cells of the Human Retina Invest. Ophthalmol. Vis. Sci., March 1, 2003; 44(3): 1237 - 1244. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Rymer, S. S. Miller, and J. L. Edelman Epinephrine-Induced Increases in [Ca2+]in and KCl-Coupled Fluid Absorption in Bovine RPE Invest. Ophthalmol. Vis. Sci., July 1, 2001; 42(8): 1921 - 1929. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. H. Quinn, J. N. Quong, and S. S. Miller Adrenergic Receptor Activated Ion Transport in Human Fetal Retinal Pigment Epithelium Invest. Ophthalmol. Vis. Sci., January 1, 2001; 42(1): 255 - 264. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
