May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Altered Light Response of Rod Photoreceptors Surviving Light Damage
Author Affiliations & Notes
  • Y. Wen
    University of Alabama at Birmingham, Birmingham, Alabama
    Neurobiology,
  • T. W. Kraft
    University of Alabama at Birmingham, Birmingham, Alabama
    Vision Sciences and Neurobiology,
  • Footnotes
    Commercial Relationships  Y. Wen, None; T.W. Kraft, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1689. doi:
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      Y. Wen, T. W. Kraft; Altered Light Response of Rod Photoreceptors Surviving Light Damage. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1689.

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

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Abstract

Purpose: : It is well known that constant light exposure can induce photoreceptor degeneration. However, it is not known if photoreceptors alter their physiology to adapt to the environmental stress caused by constant light exposure. We developed a slow light damage model in which about half of the photoreceptors are lost to study the single rod physiology after light damage.

Methods: : The rat rod physiology was documented at 3 days (R3), 5 days (R5), 15 days (R15), and 30 days (R30) after 10 days of light damage, or sham light damage for control cells. In addition to single rod recording using suction electrode, we used electroretinogram (ERG) and quantitative histology to monitor the changes of the retinal physiology and morphology.

Results: : About half of the rods are lost but there were no changes in the inner nuclear layer thickness. The Outer Segment Length was significantly shorter at R3 and R5 but by R15 OS length was normal. We found that after light damage surviving rods have lower sensitivity to light. Specifically, the I1/2 (Flash Strength that elicits half-maximal response amplitude) was increased by 65% at R3 comparing to age-matched control. However, no significant decrease in single photon response amplitude and Rmax was observed. Thereafter, sensitivity to light recovered to a level that is not different from the age-matched control group. In addition, faster recovery of the light response was observed at R3 and R5 comparing to age-matched control. Dominant Time Constant (τ) was decreased by almost half at R3, and a third at R5, but recovered to the value of the control group by R15.

Conclusions: : Our results show that transient light damage experience caused prolonged but reversible physiological changes in the surviving rods and suggest that mechanisms controlling the phototransduction cascade could be involved in this process.

Keywords: photoreceptors • degenerations/dystrophies • electrophysiology: non-clinical 
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