January 1999
Volume 40, Issue 1
Free
Articles  |   January 1999
Rod photoreceptors in infant rats with a history of oxygen exposure.
Author Affiliations
  • A B Fulton
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
  • X Reynaud
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
  • R M Hansen
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
  • C A Lemere
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
  • C Parker
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
  • T P Williams
    Department of Ophthalmology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Investigative Ophthalmology & Visual Science January 1999, Vol.40, 168-174. doi:
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    • Get Citation

      A B Fulton, X Reynaud, R M Hansen, C A Lemere, C Parker, T P Williams; Rod photoreceptors in infant rats with a history of oxygen exposure.. Invest. Ophthalmol. Vis. Sci. 1999;40(1):168-174.

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Abstract

PURPOSE: To study in an infant rat model of retinopathy of prematurity, the rod photoreceptors, which are known to have attenuated photoresponses. METHODS: Rhodopsin was extracted from whole retinas, the thickness of the rod outer segment (ROS) layer was measured, large phagosomes were counted, and the ROS ultrastructure was examined in the retinas of oxygen-exposed and control rats, ages 13 and 18 days. Rhodopsin absorbances in the ROS were measured by microspectrophotometry at age 20 days. RESULTS: The rhodopsin content did not differ significantly between the oxygen-exposed and control rats at either 13 or 18 days. The thickness of the ROS layer was equal in 13-day-old oxygen-exposed and control rats; however, at 18 days, the ROS layer was significantly thinner in the oxygen-exposed rats than in the control rats. The number of phagosomes did not vary significantly among the oxygen-exposed and control groups. Opsin immunoreactivity was seen only in the ROS layer in oxygen-exposed and control rats. The ROS were disorganized in oxygen-exposed rats. The rhodopsin absorbances of the oxygen-exposed ROS were significantly more variable and higher than in the control rats. CONCLUSIONS: Attenuation of the rod photoresponse parameters does not result simply from shortening of the outer segments and consequent low rhodopsin content. Rather, the structure of the outer segments is altered. A fault in the synthesis of the outer segments, rather than disposal of outer segment discs, is suspected.

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