May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Role of Kir4.1 and CFTR in RPE–generated components of the ERG
Author Affiliations & Notes
  • J. Wu
    Cole Eye Institute, Cleveland Clinic Fndn, Cleveland, OH
  • A.D. Marmorstein
    Ophthalmology, University of Arizona, Tucson, AZ
  • P. Kofuji
    Neuroscience, University of Minnesota, Minneapolis, MN
  • N.S. Peachey
    Cole Eye Institute, Cleveland Clinic Fndn, Cleveland, OH
    Research Service, Cleveland VAMC, Cleveland, OH
  • Footnotes
    Commercial Relationships  J. Wu, None; A.D. Marmorstein, None; P. Kofuji, None; N.S. Peachey, None.
  • Footnotes
    Support  NIH Grants EY14465, EY13160, EY12949; VA
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 809. doi:
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      J. Wu, A.D. Marmorstein, P. Kofuji, N.S. Peachey; Role of Kir4.1 and CFTR in RPE–generated components of the ERG . Invest. Ophthalmol. Vis. Sci. 2004;45(13):809.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To use mutant mice to examine the role of specific ion channels in generating the retinal pigment epithelium (RPE)–generated components of the electroretinogram (ERG). To address the potential roles of Kir4.1 in generating the c–wave and of CFTR in generating the fast oscillation, we recorded ERGs from Kir4.1 and cftr mutant mice, respectively. Methods: After overnight dark adaptation, adult mice were sedated with ketamine/xylazine and placed on a heating pad. Ag/AgCl electrodes made electrical contact with the corneal surface of each eye using capillary tubes filled with Hanks BSS. One eye was stimulated with light (full–field, 7 min duration) while the other (reference) eye was shielded. Signals were differentially amplified (dc–100 Hz), digitized (20 Hz) and stored off–line. Results: ERG c–waves of Kir4.1 +/– heterozygous mice were larger than those of Kir4.1 +/+ littermates. There were no other differences in the ERGs of Kir4.1 +/– and Kir4.1 –/– mice. Aside from a modest reduction in overall amplitude, ERGs recorded from cftr –/– mice were not different from cftr +/– or cftr +/+ littermates. Conclusions: The c–wave increase in Kir4.1 +/– mice is likely to reflect a reduction in the amplitude of slow PIII, an ERG component that is opposite in polarity to the cornea–positive c–wave. The presence of a normal fast oscillation in cftr –/– mice indicates that Cl– conductance through CFTR is unlikely to underlie this ERG component. We plan to extend this analysis to other mutant mice involving RPE ion channels.

Keywords: retinal pigment epithelium • electroretinography: non–clinical • transgenics/knock–outs 

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