TY - JOUR
T1 - A light-evoked interaction of apical and basal membranes of retinal pigment epithelium
T2 - c-wave and light peak
AU - Linsenmeier, R. A.
AU - Steinberg, R. H.
PY - 1983
Y1 - 1983
N2 - An increase in the amplitude of the electroretinogram (ERG) c-wave during the light peak was first observed in humans. The present work investigated the cellular mechanism of this phenomenon in the intact cat retina. DC recordings were made between an electrode in the vitreous humor and a reference behind the eye. Repeated flashes of diffuse white light elicited a light peak on which ERGs were superimposed. The c-wave increased in amplitude during the light peak, and the magnitude of the change was directly related to light-peak amplitude. Microelectrodes placed in the subretinal space, outside the apical membrane of the retinal pigment epithelium (RPE), differentially recorded the two components of the c-wave, retinal and pigment epithelial. The variation of the vitreal c-wave during the light peak resulted from a change in the component of the c-wave generated by the RPE rather than the component generated by the neural retina. The RPE component of the c-wave is the difference between a hyperpolarization of the apical membrane, caused by a light-evoked decrease in extracellular potassium, and a hyperpolarization of the basal membrane, caused by electrical shunting of the apical response. There are theoretically several ways in which the RPE component of the c-wave could increase. Intracellular recordings from RPE cells showed that the variation was due to a decrease in the resistance of the basal membrane (R(ba)) during the light peak. Two kinds of evidence contributed to this finding. First, the hyperpolarization of both membranes were reduced during the light peak. The c-wave grew during the light peak, despite the reduction in membrane responses, because the basal hyperpolarization was reduced more than the apical. Second, the voltage responses to current pulses injected across the tissue showed that there was an increase in the ratio of apical to basal membrane resistance and a decrease in the equivalent resistance of the epithelium. These findings would be expected only if R(ba) decreased. (The origin of the resistance change, first found in the gecko, is still unknown). This phenomenon represents one type of light-evoked interaction between the apical and basal membranes: a basal resistance change modifies the apical membrane potential. This may serve as a model for changes in c-wave amplitude in other conditions and may be important in its own right in modulating transport or other membrane-potential-dependent functions of the pigment epithelium. Since the c-wave varies with the light peak in humans as well, the present results indicate that the human light peak also must be accompanied by a change in basal membrane resistance. In addition to the variation of the c-wave during the light peak, changes in c-wave amplitude due to light adaptation were observed. These changes occurred in both the retinal and RPE components of the c-wave and had relatively little influence on the amplitude of the vitreal c-wave.
AB - An increase in the amplitude of the electroretinogram (ERG) c-wave during the light peak was first observed in humans. The present work investigated the cellular mechanism of this phenomenon in the intact cat retina. DC recordings were made between an electrode in the vitreous humor and a reference behind the eye. Repeated flashes of diffuse white light elicited a light peak on which ERGs were superimposed. The c-wave increased in amplitude during the light peak, and the magnitude of the change was directly related to light-peak amplitude. Microelectrodes placed in the subretinal space, outside the apical membrane of the retinal pigment epithelium (RPE), differentially recorded the two components of the c-wave, retinal and pigment epithelial. The variation of the vitreal c-wave during the light peak resulted from a change in the component of the c-wave generated by the RPE rather than the component generated by the neural retina. The RPE component of the c-wave is the difference between a hyperpolarization of the apical membrane, caused by a light-evoked decrease in extracellular potassium, and a hyperpolarization of the basal membrane, caused by electrical shunting of the apical response. There are theoretically several ways in which the RPE component of the c-wave could increase. Intracellular recordings from RPE cells showed that the variation was due to a decrease in the resistance of the basal membrane (R(ba)) during the light peak. Two kinds of evidence contributed to this finding. First, the hyperpolarization of both membranes were reduced during the light peak. The c-wave grew during the light peak, despite the reduction in membrane responses, because the basal hyperpolarization was reduced more than the apical. Second, the voltage responses to current pulses injected across the tissue showed that there was an increase in the ratio of apical to basal membrane resistance and a decrease in the equivalent resistance of the epithelium. These findings would be expected only if R(ba) decreased. (The origin of the resistance change, first found in the gecko, is still unknown). This phenomenon represents one type of light-evoked interaction between the apical and basal membranes: a basal resistance change modifies the apical membrane potential. This may serve as a model for changes in c-wave amplitude in other conditions and may be important in its own right in modulating transport or other membrane-potential-dependent functions of the pigment epithelium. Since the c-wave varies with the light peak in humans as well, the present results indicate that the human light peak also must be accompanied by a change in basal membrane resistance. In addition to the variation of the c-wave during the light peak, changes in c-wave amplitude due to light adaptation were observed. These changes occurred in both the retinal and RPE components of the c-wave and had relatively little influence on the amplitude of the vitreal c-wave.
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U2 - 10.1152/jn.1983.50.1.136
DO - 10.1152/jn.1983.50.1.136
M3 - Article
C2 - 6875643
AN - SCOPUS:0020571111
SN - 0022-3077
VL - 50
SP - 136
EP - 147
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 1
ER -