May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Detailed histopathologic characterization of the retinopathy, globe enlarged (rge) chick
Author Affiliations & Notes
  • S.M. Petersen–Jones
    Department of Small Animal Clinical Sciences,
    Michigan State University, East Lansing, MI
  • R. Cernuda–Cernuda
    Department of Morphology and Cellular Biology, University of Oviedo, Oviedo, Spain
  • A. Fischer
    Department of Neuroscience, The Ohio State University, Columbus, OH
  • W. DeGrip
    Department of Biochemistry, University of Nijmegen, Nijmegen, The Netherlands
  • M. Kiuppel
    Diagnostic Center for Population and Animal Health,
    Michigan State University, East Lansing, MI
  • F. Montiani–Ferreira
    Department of Small Animal Clinical Sciences,
    Michigan State University, East Lansing, MI
  • Footnotes
    Commercial Relationships  S.M. Petersen–Jones, None; R. Cernuda–Cernuda, None; A. Fischer, None; W. DeGrip, None; M. Kiuppel, None; F. Montiani–Ferreira, None.
  • Footnotes
    Support  MSU Genetic Research Fund, CAPES
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3589. doi:
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      S.M. Petersen–Jones, R. Cernuda–Cernuda, A. Fischer, W. DeGrip, M. Kiuppel, F. Montiani–Ferreira; Detailed histopathologic characterization of the retinopathy, globe enlarged (rge) chick . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3589.

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

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Abstract

Abstract: : Purpose: To characterize the morphologic retinal changes in the rge chicken. Methods: Rge–affected and age matched control retinas were examined from hatch up to 730 days of age. Thickness of retinal layers at six retinal regions was measured from plastic embedded sections. Morphological features were examined on semithin sections by light microscropy and on ultrathin sections by transmission electron microscopy. Immunohistochemistry was performed using a variety of antibodies including opsin and GFAP. Results:The earliest changes detected were morphological abnormalities in the outer plexiform layer. The normal bi–layered arrangement of photoreceptor synaptic terminal was absent at hatch. Rod spherules and cone pedicles were disorganized and swollen. Synaptic ribbons were reduced in numbers and abnormal synaptic vesicles were detected by 7 days of age. Abnormal localization of the rough endoplasmic reticulum of the photoreceptors inner segments was observed at hatch and was the site of glycogen deposition apparent by 14 days of age. By the same age the rge retina was thinner than that of controls with a reduced number of rod photoreceptors outer segments per unit length of retina. Rod inner segments showed increased opsin immunoreactivity by 14 days of age and in older birds mislocalized opsin immunoreactivity was also observed in the OPL. As the disease progressed there was increased GFAP staining and glial cell processes became more prominent in the ONL and OPL. Conclusions:Alterations in photoreceptor synaptic terminals were an early and progressive change present during the period of vision loss in rge–affected birds. Slight, but significant, retinal thinning was present by 14 days of age, but marked retinal thinning did not develop until after functional vision loss had been present for some weeks. We believe that globe enlargement explains some of the retinal thinning. There is not sufficient loss of photoreceptors to account for the blindness, however if the alterations in synaptic terminals reflect synaptic dysfunction this may explain vision loss and altered (but not extinguished) ERG responses that are characteristic of the rge phenotype.

Keywords: retinal degenerations: hereditary • retina: distal (photoreceptors, horizontal cells, bipolar cells) • microscopy: light/fluorescence/immunohistochemistry 
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