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S- and M-Cone Electroretinograms in rd7 Mice with NR2E3 Gene Mutation

  • Shinji Ueno
  • Mineo Kondo
  • Asahiko Takahashi
  • Yozo Miyake
Conference paper
  • 143 Downloads
Part of the Keio University International Symposia for Life Sciences and Medicine book series (KEIO, volume 11)

Abstract

Earlier studies have shown that the alterations of the visual function in rd7 mice result from a deletion in the photoreceptor cell-specific nuclear receptor gene, Nr2e3 [1]. Mutations of this gene have been associated with the enhanced S-cone syndrome (ESCS) in humans [2]. Immunohistological studies also showed that the rd7 retina has an increased number of S-cone cells [3]. The purpose of this study was to examine the physiological properties of the S- and M-cones in rd7 mice electrophysiologically.

Key words

Electroretinogram rd7 mice S-cone 

References

  1. 1.
    Akhmedov NB, Piriev NI, Chang B, et al. (2000) A deletion in a photoreceptor-specific nuclear receptor mRNA causes retinal degeneration in the rd7 mouse. Proc Natl Acad Sci USA 97: 5551–5556PubMedCrossRefGoogle Scholar
  2. 2.
    Haider NB, Jacobson SG, Cideciyan AV, et al. (2000) Mutation of a nuclear receptor gene, NR2E3, causes enhanced S cone syndrome, a disorder of retinal cell fate. Nat Genet 24: 127–131PubMedCrossRefGoogle Scholar
  3. 3.
    Haider NB, Naggert JK, Nishina PM (2001) Excess cone cell proliferation due to lack of a functional NR2E3 causes retinal dysplasia and degeneration in rd7/rd7 mice. Hum Mol Genet 10: 1619–1626PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Tokyo 2003

Authors and Affiliations

  • Shinji Ueno
    • 1
  • Mineo Kondo
    • 1
  • Asahiko Takahashi
    • 1
  • Yozo Miyake
    • 1
  1. 1.Department of OphthalmologyNagoya University School of MedicineShowa-ku, NagoyaJapan

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