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1 Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
2 Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH, USA; Research Service, Cleveland VA Medical Center, Cleveland, OH, USA
3 Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH, USA; Ophthalmology, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: peachen{at}ccf.org.
In response to light, the retinal pigment epithelium (RPE) generates a series of slow potentials that can be recorded as the c-wave, fast oscillation (FO) and light peak (LP) of the electroretinogram (ERG). As these potentials can be related to specific cellular events, they provide information about RPE function and how that may be altered by disease or experimental manipulation. In the present study we describe a noninvasive means for recording the light-evoked responses of the mouse RPE, and use this to define the stimulus-response properties of the major components in three inbred strains of mice (BALBc/ByJ; C57BL/6J; 129/SvJ) and two mouse mutants that reduce activity in the rod pathway. All of the major ERG components generated by the RPE are readily measured in the mouse. In albino strains (BALBc/ByJ; 129/SvJ) the intensity-response functions for the c-wave, FO and LP are shifted toward lower intensities in comparison to those for C57BL/6J mice. Each of these components was markedly reduced in mice lacking transducin where rod phototransduction is interrupted, indicating that they reflect primarily rod photoreceptor activity. All components were observed in no b-wave (nob) mutant mice, indicating that inner retinal activity does not make a major contribution to these potentials. Further studies of mutant mice will allow us to define the functional consequences of gene manipulation on RPE function and to evaluate specific hypotheses regarding the generation of ERG components.
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