October 1966
Volume 5, Issue 5
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Articles  |   October 1966
Retinal Damage by Light in Rats
Author Affiliations
  • WERNER K. NOELL
    Department of Physiology and the Neurosensory Laboratory, State University of New York at Buffalo, School of MedicineBuffalo, N. Y.
  • VIRGIL S. WALKER
    Department of Physiology and the Neurosensory Laboratory, State University of New York at Buffalo, School of MedicineBuffalo, N. Y.
  • BOK SOON KANG
    Department of Physiology and the Neurosensory Laboratory, State University of New York at Buffalo, School of MedicineBuffalo, N. Y.; Postdoctoral Fellow from the Department of Physiology, Yonsei University, Seoul, Korea
  • STEVEN BERMAN
    Department of Physiology and the Neurosensory Laboratory, State University of New York at Buffalo, School of MedicineBuffalo, N. Y.
Investigative Ophthalmology & Visual Science October 1966, Vol.5, 450-473. doi:
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      WERNER K. NOELL, VIRGIL S. WALKER, BOK SOON KANG, STEVEN BERMAN; Retinal Damage by Light in Rats. Invest. Ophthalmol. Vis. Sci. 1966;5(5):450-473.

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

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Abstract

The retina of laboratory rats is affected irreversibly by intense light applied for less than 1 hour or for up to 2 days depending upon experimental conditions. Exposure of unanesthetized and unrestrained animals was in chambers surrounded by a green filter and circular fluorescent lamps of a nominal brightness of 2,040 footlamberts. Eyes of anesthetized animals were exposed diffusely to either the light from a 100 w. zirconium arc passing through filters or monochromatic light of various wavelengths. Irreversible reduction in ERG amplitudes and degeneration of visual cells and pigment epithelium indicated the severity of the light damage. The effect was very dependent upon the body (eye) temperature during exposure. Hyperthermia greatly accelerated and intensified the damaging action of light and for this reason most experiments reported in this paper were performed at a high body temperature. At a body temperature around 104° F. severe damage was produced with exposures to 5 to 10 µw per square centimeter retina for 1 hour. The minimal damaging dose at a high temperature was estimated to be about 1 µw per square centimeter. The action spectrumof the damaging effect approximated that of visual excitation as measured by the ERG. Hooded (pigmented) animals were no more affected than albinos of different strains. Recovery in the dark from a just subliminally damaging dose of light at a high body temperature required about 24 hours and was preceded by a period of time during which the retina was "sensitized" to an additional dose. Duringjrrfollowing exposure to light at a high body temperature visual cell and pigiiient_epithelial_dmxage developed about simultaneously and was first indicated bu pyknosis and cell swelling followed rapidly by the dissolution of nuclei and cytoplasm. The crucial reaction in producing the damage is considered a "dark-reaction" initiated by light of an intensity which bleaches measurabLiirhodopsin. Hypotheses on the reaction sequence which leads to damage are briefly discussed.

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