scholarly journals Apical and basal membrane ion transport mechanisms in bovine retinal pigment epithelium.

1991 ◽  
Vol 435 (1) ◽  
pp. 439-463 ◽  
Author(s):  
D P Joseph ◽  
S S Miller
Keyword(s):  
Retinal Pigment Epithelium ◽  
Ion Transport ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basal Membrane ◽  
Transport Mechanisms ◽  
Membrane Ion Transport

Lactate transport mechanisms at apical and basolateral membranes of bovine retinal pigment epithelium

1994 ◽  
Vol 267 (6) ◽  
pp. C1561-C1573 ◽  
Author(s):  
E. Kenyon ◽  
K. Yu ◽  
M. La Cour ◽  
S. S. Miller
Keyword(s):  
Retinal Pigment Epithelium ◽  
Short Circuit ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basolateral Membrane ◽  
Open Circuit ◽  
Subretinal Space ◽  
Transport Mechanisms ◽  
Lactate Transport ◽  
Space Volume

The isolated bovine retinal pigment epithelium actively transports lactate from the apical to the basal bath. Net short-circuit [14C]lactate flux in 20 mM lactate was 0.46 +/- 0.09 mu eq.cm-2.h-1 (n = 8). In open circuit, with a physiological lactate gradient, net [14C]lactate flux was 0.66-1.31 mu eq.cm-2.h-1 (n = 3). Lactate in the apical bath caused intracellular acidifications that were saturable, apparently stereospecific, and reduced in magnitude by several H-lactate cotransport inhibitors. In the basal bath, lactate caused intracellular alkalinizations that were dependent on the presence of Na. In short circuit, 20 mM lactate in both baths reversed the direction of net transepithelial 22Na transport from secretion to absorption, suggesting the presence of basolateral Na-lactate cotransport moving lactate out of the cells. Outwardly directed Na-lactate cotransport requires a lactate:Na stoichiometry > 1.4:1, consistent with the coupled movement of Na, lactate, and net negative charge across the basolateral membrane. Intracellular microelectrode recordings showed that basal lactate hyperpolarized and apical lactate depolarized the basolateral membrane. For lactate absorption, this is a novel arrangement of membrane proteins:luminal H-lactate cotransport and serosal electrogenic Na:(n)lactate cotransport. Lactate transport across the retinal pigment epithelium may play an important role in regulating retinal metabolism and subretinal space volume and composition.

scholarly journals Changes in apical [K+] produce delayed basal membrane responses of the retinal pigment epithelium in the gecko.

1984 ◽  
Vol 83 (2) ◽  
pp. 193-211 ◽  
Author(s):  
E R Griff ◽  
R H Steinberg
Keyword(s):  
Membrane Potential ◽  
Retinal Pigment Epithelium ◽  
Apical Membrane ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basal Membrane ◽  
Subretinal Space ◽  
Bathing Solution ◽  
Subsequent Decrease ◽  
Opposite Sequence

We describe here a new retinal pigment epithelium (RPE) response, a delayed hyperpolarization of the RPE basal membrane, which is initiated by the light-evoked decrease of [K+]o in the subretinal space. This occurs in addition to an apical hyperpolarization previously described in cat (Steinberg et al., 1970; Schmidt and Steinberg, 1971) and in bullfrog (Oakley et al., 1977; Oakley, 1977). Intracellular and extracellular potentials and measurements of subretinal [K+]o were recorded from an in vitro preparation of neural retina-RPE-choroid from the lizard Gekko gekko in response to light. Extracellularly, the potential across the RPE, the transepithelial potential (TEP), first increased and then decreased during illumination. Whereas the light-evoked decrease in [K+]o predicted the increase in TEP, the subsequent decrease in TEP was greater than predicted by the reaccumulation of [K+]o. Intracellular RPE recordings showed that a delayed hyperpolarization generated at the RPE basal membrane produced the extra TEP decrease. At light offset, the opposite sequence of membrane potential changes occurred. RPE responses to changes in [K+]o were studied directly in the isolated gecko RPE-choroid. Decreasing [K+]o in the apical bathing solution produced first a hyperpolarization of the apical membrane, followed by a delayed hyperpolarization of the basal membrane, a sequence of membrane potential changes identical to those evoked by light. Increasing [K+]o produced the opposite sequence of membrane potential changes. In both preparations, the delayed basal membrane potentials were accompanied by changes in basal membrane conductance. The mechanism by which a change in extracellular [K+] outside the apical membrane leads to a polarization of the basal membrane remains to be determined.

Basolateral membrane Cl- and K+ conductances of the dark-adapted chick retinal pigment epithelium

1993 ◽  
Vol 70 (4) ◽  
pp. 1656-1668 ◽  
Author(s):  
R. P. Gallemore ◽  
E. Hernandez ◽  
R. Tayyanipour ◽  
S. Fujii ◽  
R. H. Steinberg
Keyword(s):  
Retinal Pigment Epithelium ◽  
Time Course ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basolateral Membrane ◽  
Basal Membrane ◽  
Diffusion Potential ◽  
Ion Concentration ◽  
Concentration Changes ◽  
Cl Conductance

1. We characterized the basolateral membrane Cl- and K+ conductances of the dark-adapted chick neural retina-retinal pigment epithelium (RPE)-choroid preparation. Conventional microelectrodes were used to measure apical (V(ap)) and basolateral (Vba) membrane voltage, and double-barreled Cl- and K+ selective microelectrodes were used to follow the time course and magnitude of ion concentration changes outside the basolateral (basal) membrane. 2. In response to a fivefold decrease in basal [Cl-]o, Vba rapidly depolarized by 6.4 +/- 0.7 (SE) mV, and the apparent resistance of the basolateral membrane (Rba) increased. The Cl- channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) suppressed the Vba depolarization by 40% and blocked the Rba increase. Estimates of the relative Cl- conductance (transference number, TCl) from the DIDS-sensitive component of the Cl- diffusion potential gave an average value for TCl of 0.22 +/- 0.03. 3. Further evidence for a Cl- conductance was obtained by measuring changes in intracellular Cl- activity (aCli) induced by transtissue current. Depolarizing Vba elevated aiCl, whereas hyperpolarizing Vba had the opposite effect, consistent with conductive Cl- movement across the basal membrane. TCl estimated from these data averaged 0.23 +/- 0.02. 4. In response to a sixfold increase in basal [K+]o, Vba depolarized 6.1 +/- 0.8 mV. The amplitude of this K+ diffusion potential was inhibited 44 and 67% by 5 and 10 mM Ba2+, respectively. TK was estimated to be 0.61 +/- 0.05. 5. The rapid c-wave membrane hyperpolarizations in response to the light-evoked decrease in subretinal [K+]o were used to calculate the equivalent resistances of the apical membrane (R(ap)), basolateral membrane (Rba), and the paracellular shunt pathway (Rs). They were 152 +/- 10, 615 +/- 38, and 138 +/- 7 omega.cm2 (n = 11 tissues), respectively. From these data the equivalent electromotive force for the basal (Eba) and apical (Eap) membranes were estimated to be -45 +/- 2 and -77 +/- 1 mV, respectively. This estimate of Eba is in the range of that predicted from our estimates of TCl and TK, indicating that, in the dark-adapted chick retina, the resting conductance of the basal membrane can largely be accounted for by the Cl- and K+ conductances described here.

scholarly journals Cyclic AMP modulation of ion transport across frog retinal pigment epithelium. Measurements in the short-circuit state.

1984 ◽  
Vol 83 (6) ◽  
pp. 853-874 ◽  
Author(s):  
S Miller ◽  
D Farber
Keyword(s):  
Retinal Pigment Epithelium ◽  
Cyclic Amp ◽  
Ion Transport ◽  
Apical Membrane ◽  
Short Circuit ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basolateral Membrane ◽  
Active Absorption ◽  
Apical Side

In the frog retinal pigment epithelium (RPE), the cellular levels of cyclic AMP (cAMP) were measured in control conditions and after treatment with substances that are known to inhibit phosphodiesterase (PDE) activity (isobutyl-1-methylxanthine, SQ65442) or stimulate adenylate cyclase activity (forskolin). The cAMP levels were elevated by a factor of 5-7 compared with the controls in PDE-treated tissues and by a factor of 18 in forskolin-treated tissues. The exogenous application of cAMP (1 mM), PDE inhibitors (0.5 mM), or forskolin (0.1 mM) all produced similar changes in epithelial electrical parameters, such as transepithelial potential (TEP) and resistance (Rt), as well as changes in active ion transport. Adding 1 mM cAMP to the solution bathing the apical membrane transiently increased the short-circuit current (SCC) and the TEP (apical side positive) and decreased Rt. Microelectrode experiments showed that the elevation in TEP is due mainly to a depolarization of the basal membrane followed by, and perhaps also accompanied by, a smaller hyperpolarization of the apical membrane. The ratio of the apical to the basolateral membrane resistance increased in the presence of cAMP, and this increase, coupled with the decrease in Rt and the basolateral membrane depolarization, is consistent with a conductance increase at the basolateral membrane. Radioactive tracer experiments showed that cAMP increased the active secretion of Na (choroid to retina) and the active absorption of K (retina to choroid). Cyclic AMP also abolished the active absorption of Cl across the RPE. In sum, elevated cellular levels of cAMP affect active and passive transport mechanisms at the apical and basolateral membranes of the bullfrog RPE.

scholarly journals Delayed basal hyperpolarization of cat retinal pigment epithelium and its relation to the fast oscillation of the DC electroretinogram.

1984 ◽  
Vol 83 (2) ◽  
pp. 213-232 ◽  
Author(s):  
R A Linsenmeier ◽  
R H Steinberg
Keyword(s):  
Retinal Pigment Epithelium ◽  
Time Course ◽  
Apical Membrane ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basal Membrane ◽  
Fast Oscillation ◽  
Light Peak ◽  
Absorption Of Light ◽  
Intermediate Time

Previous work has shown that the cat retinal pigment epithelium (RPE) is the source of two potential changes that follow the absorption of light by photoreceptors: a hyperpolarization of the apical membrane, peaking in 2-4 s, which leads to the RPE component of the electroretinogram (ERG) c-wave, and a depolarization of the basal membrane, peaking in 5 min, which leads to the light peak. This paper describes a new basal membrane response of intermediate time course, called the delayed basal hyperpolarization. Isolation of this response from other RPE potentials showed that with maintained illumination the hyperpolarization begins approximately 2 s after light onset, peaks in 20 s, and slowly ends as the membrane repolarizes over the next 60 s. The delayed basal hyperpolarization is very small for stimuli less than 4 s in duration and grows with duration, becoming approximately 15% as large as the preceding apical hyperpolarization with stimuli longer than 20 s. Extracellularly, this response contributes to the transepithelial potential (TEP) across the RPE. In response to light the TEP first rises to a peak, the c-wave, as the apical membrane hyperpolarizes. For stimuli longer than approximately 4 s, the decline of the TEP from the peak of the c-wave results partly from the recovery of apical membrane potential and partly from the delayed basal hyperpolarization. For long periods of illumination (300 s) the delayed basal hyperpolarization leads to a trough in the TEP between the c-wave and light peak. This trough is largely responsible for a corresponding trough in vitreal recordings, which has been called the "fast oscillation." The term "fast oscillation" has also been used to denote the sequence of potential changes resulting from repeated stimuli approximately 1 min in duration. In addition to the delayed basal hyperpolarization, such responses also contain a basal off-response, a delayed depolarization.

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