May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Role for bestrophin in generating the light peak of the DC Electroretinogram
Author Affiliations & Notes
  • R.P. Gallemore
    Retina–Vitreous Associates, Los Angeles, CA
    Jules Stein Eye Institute, UCLA, Los Angeles, CA
  • D. Bok
    Jules Stein Eye Institute, UCLA, Los Angeles, CA
  • J. Hu
    Jules Stein Eye Institute, UCLA, Los Angeles, CA
  • F. Maruiwa
    Jules Stein Eye Institute, UCLA, Los Angeles, CA
  • J. Yocom
    Ophthalmology, University of Arizona, Tucson, AZ
  • O. Strauss
    Institut fuer Klinische Physiologie, Universitaetsklinikum Benjamin Franklin, Freie Universitaet Berlin, Berlin, Germany
  • N. Peachey
    Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, OH
  • A.D. Marmorstein
    Ophthalmology, University of Arizona, Tucson, AZ
  • Footnotes
    Commercial Relationships  R.P. Gallemore, None; D. Bok, None; J. Hu, None; F. Maruiwa, None; J. Yocom, None; O. Strauss, None; N. Peachey, None; A.D. Marmorstein, None.
  • Footnotes
    Support  NIH Grants EY13160, EY13847, EY444
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1761. doi:
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      R.P. Gallemore, D. Bok, J. Hu, F. Maruiwa, J. Yocom, O. Strauss, N. Peachey, A.D. Marmorstein; Role for bestrophin in generating the light peak of the DC Electroretinogram . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1761.

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

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Abstract

Abstract: : Purpose: To present a model for generation of the light peak of the dc electroretinogram. Methods: Conventional electrophysiologic techniques were used on cultured human RPE monolayers. To assess the role of L–type Ca channels on the light peak DC electroretinograms were recorded from rats injected with nimodipine. Results: In human RPE, apical ATP produces a sustained activation of Cl channels that approximates the time course of the light peak in situ. We found that the voltage response depends on purinergic receptors, external Ca entry, and is inhibited by basal NPPB, apical DIDS, apical ionomycin, but not by BAPTA or suramin. Agonist sensitivity was: ATP>UTP. In patch clamp studies reported separately, bestrophin altered voltage sensitivity of Ca channels allowing Ca channel activation at more physiologic resting potentials. The L–type Ca channel blocker nimodipine significantly reduced the amplitude of the light peak in situ without causing a reduction in a– or b– wave amplitude, or heart rate. Conclusions: ATP stimulation of RPE cells induces a sustained depolarizing Ca–dependent Cl conductance across the basal membrane of the RPE. Since depletion of intracellular Ca does not prevent this effect, Ca must be drawn from the extracellular pool. The effects of nimodipine on the light peak, indicate that L–type channels are involved in the light peak response. Since bestrophin alters the voltage sensitivity of L–type Ca channels, we propose that the light peak is sustained by the entry of extracellular calcium through L–type channels, and that bestrophin may function as the gain switch for the light peak via its ability to regulate L–type Ca channel activity.

Keywords: electroretinography: clinical • retinal pigment epithelium • electrophysiology: clinical 
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