December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Light Induced Photoreceptor Apoptosis: Is Phototransduction Involved?
Author Affiliations & Notes
  • A Wenzel
    Lab Retinal Cell Biology University Hospital Zurich Zurich Switzerland
  • C Grimm
    Lab Retinal Cell Biology University Hospital Zurich Zurich Switzerland
  • MS Obin
    Nutrition and Vision Research Tufts University Boston MA
  • MI Simon
    Div of Biology California Inst of Technology Pasadena CA
  • J Lem
    Ophthalmology New England Medical Center Boston MA
  • CE Remé
    Lab Retinal Cell Biology University Hospital Zurich Zurich Switzerland
  • Footnotes
    Commercial Relationships   A. Wenzel, None; C. Grimm, None; M.S. Obin, None; M.I. Simon, None; J. Lem, None; C.E. Remé, None. Grant Identification: Swiss National Science Fdn., German Research Council, Velux Fdn., Switzerland
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3720. doi:
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    • Get Citation

      A Wenzel, C Grimm, MS Obin, MI Simon, J Lem, CE Remé; Light Induced Photoreceptor Apoptosis: Is Phototransduction Involved? . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3720.

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

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Abstract

Abstract: : Purpose: Light induced apoptosis of rod-photoreceptors is mediated by rhodopsin and involves activation of the transcription factor AP-1. However, the signaling pathways leading from photon absorption by rhodopsin to the initiation of the death program and/or activation of AP-1 are unknown. Evidence from mice deficient for arrestin (Arr-/-) or rhodopsin kinase (Rhok-/-) - both involved in phototransduction shut off - suggested that undamped phototransduction increases a photoreceptor's sensitivity to light damage. Thus, phototransduction may be a way to mediate light damage. Here we analyze mice deficient for the transducin alpha-subunit (Gnat1-/-), which lack rod phototransduction, and Arr-/- / Rhok-/- doubly mutant mice to test for an involvement of phototransduction in white light induced apoptosis of photoreceptors. Methods: Mice were exposed to 3 different white light regimens: (1) 5000lux for 1-30 minutes (2) 1700lux for 1 week (3) 800lux 12:12h cyclic for 5 month. Light damage was analyzed by retinal morphology. Electromobility shift assays (EMSA) were employed to test for an involvement of AP-1. Results: With regimen (1), Arr-/- / Rhok-/- doubly mutant mice were extremely sensitive to light damage with apoptosis of photoreceptors occurring after 2 minutes of light exposure, thus being at least 10 times more sensitive than a corresponding wild type mouse. Gnat1-/- mice showed light damage after 20-30 minutes of light exposure, thus being indistinguishable from wild type mice. In Arr-/- / Rhok-/- and in Gnat1-/- mice light induced AP-1 DNA binding activity as in wild type mice. With regimen (2) and (3), Gnat1-/- and Gnat1+/+ mice displayed comparable patterns of photoreceptor cell loss. Conclusion: Death signals generated by rhodopsin upon absorption of a lethal dose of photons are not mediated via phototransduction. Alternative pathways must exist that lead from bleaching of rhodopsin via activation of AP-1 to cell death. Those pathways may be modulated by the interaction of rhodopsin with arrestin and / or rhodopsin kinase.

Keywords: 341 cell death/apoptosis • 561 retinal degenerations: cell biology • 580 signal transduction 
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