May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Characterization of Retinal Degeneration in SOD1-Deficient Mice: Electrophysiology and Histopathology
Author Affiliations & Notes
  • Y. Imamura
    Ophthalmology, Keio Univ School of Medicine, Shinjuku-Ku, Japan
  • M. Hirasawa
    Ophthalmology, Keio Univ School of Medicine, Shinjuku-Ku, Japan
  • K. Hashizume
    Ophthalmology, Keio Univ School of Medicine, Shinjuku-Ku, Japan
  • S. Noda
    Tokai Univ School of Nursing, Kanagawa, Japan
  • T. Shirasawa
    Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan
  • K. Shinoda
    National Institute of Sensory Organ, Tokyo, Japan
  • Y. Miyake
    National Institute of Sensory Organ, Tokyo, Japan
  • K. Tsubota
    Ophthalmology, Keio Univ School of Medicine, Shinjuku-Ku, Japan
  • Footnotes
    Commercial Relationships Y. Imamura, None; M. Hirasawa, None; K. Hashizume, None; S. Noda, None; T. Shirasawa, None; K. Shinoda, None; Y. Miyake, None; K. Tsubota, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 21. doi:
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      Y. Imamura, M. Hirasawa, K. Hashizume, S. Noda, T. Shirasawa, K. Shinoda, Y. Miyake, K. Tsubota; Characterization of Retinal Degeneration in SOD1-Deficient Mice: Electrophysiology and Histopathology. Invest. Ophthalmol. Vis. Sci. 2007;48(13):21.

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

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Abstract

Purpose:: To examine the retinal function of mice lacking Cu,Zn-superoxide dismutase (SOD1) using electroretinogram and histology.

Methods:: Scotopic,photopic and flicker electroretinogram (ERG) were recorded from wild-type and Sod1-/- mice of different ages. The sensory retina was also examined histologically.

Results:: Aged Sod1-/- mice showed a decrease in the amplitude ofERGs. Retinal dysfunction appeared to progress with age. Histology revealed that retinal thinning and pigment cell migration co-existed with choroidal neovascularization (CNV) in aged Sod1-/- mice.

Conclusions:: Recently, we have reported that aged Sod1-/- mice showed drusen, thickened Bruch membrane, and CNV. Because retinal degeneration is a hallmark of dry type of age-related macular degeneration (AMD), our present results suggest Sod1-/-mouse be considered as a model of either wet or dry type of AMD. Moreover, these observations imply that these two conditions can be caused by deficiency of single gene.

Keywords: age-related macular degeneration • electrophysiology: non-clinical • retinal degenerations: cell biology 
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