May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
A Novel Neuroprotective Effect of Naloxone in Light-Induced Photoreceptor Degeneration Through Inhibiting Activation of Retinal Microglia
Author Affiliations & Notes
  • Y. Ni
    Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China
  • G.-Z. Xu
    Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China
  • W.-Z. Hu
    Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, Indiana
  • P.-Q. Zhao
    Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China
  • L. Shi
    Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China
  • Y.-W. Qin
    Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China
  • Footnotes
    Commercial Relationships  Y. Ni, None; G. Xu, None; W. Hu, None; P. Zhao, None; L. Shi, None; Y. Qin, None.
  • Footnotes
    Support  the National Key Basic Research Program of China(973 Program)
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4413. doi:https://doi.org/
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      Y. Ni, G.-Z. Xu, W.-Z. Hu, P.-Q. Zhao, L. Shi, Y.-W. Qin; A Novel Neuroprotective Effect of Naloxone in Light-Induced Photoreceptor Degeneration Through Inhibiting Activation of Retinal Microglia. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4413. doi: https://doi.org/.

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

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Abstract

Purpose: : To study the role of microglia activation and migration in light-induced photoreceptor degeneration and evaluate the novel neuroprotective effect of naloxone as a microglia inhibitor.

Methods: : Sprague-Dawley rats received light exposure at 2500 lux for 24 hours. Daily intraperitoneal injection of naloxone or PBS was started 2 days before light exposure and lasted for 2 weeks. TUNEL staining and anti-OX42 antibody were used to detect DNA fragmentation and label retinal microglia. Western-blot was used to evaluate the protein level of IL-1ß in retina. Retinal histology, immunohistochemistry and electroretinography were performed to evaluate the effect of naloxone in light-induced photoreceptor degeneration.

Results: : TUNEL-positive cells were noted in the outer nuclear layer (ONL) as early as 2 hours and reached the peak at 24 hours after light exposure. OX42-positive microglia occurred in the ONL and subretinal space at 6 hours, peaked at 3 days, and changed morphologically from the resting ramified to the activated amoeboid. The protein expression of IL-1ß was also increased significantly at 3 days. Compared to the PBS control group, TUNEL-positive cells in the ONL were significantly decreased in the naloxone-treated group at 3 and 7 days but no different at 1 day with microglia migrated in the outer retina decreased at 3 days; and the thickness of ONL and the amplitudes of dark-adapted a- and b-waves were also well preserved at 14 days.

Conclusions: : Activation and migration of retinal microglia, as well as expression of neurotoxic factor(IL-1ß), coincides with photoreceptor apopotosis, suggesting activated microglia play a major role in photoreceptor degeneration. Naloxone protects against further degeneration of photoreceptors after light damage by inhibiting the microglial activation.

Keywords: microglia • photoreceptors • degenerations/dystrophies 
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