May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Calpain and N–Methyl–D–Aspartate (NMDA)–Induced Excitotoxicity in Rat Retina
Author Affiliations & Notes
  • J.M. Kwong
    Jules Stein Eye Institute, Univ California Los Angeles, Los Angeles, CA
    Ophthalmology & Visual Science, Chinese Univ Hong Kong, Hong Kong, Hong Kong Special Administrative Region of China
  • K. Chiu
    Ophthalmology & Visual Science, Chinese Univ Hong Kong, Hong Kong, Hong Kong Special Administrative Region of China
    Anatomy, Univ Hong Kong, Hong Kong, Hong Kong Special Administrative Region of China
  • W.W. Y. Li
    Ophthalmology & Visual Science, Chinese Univ Hong Kong, Hong Kong, Hong Kong Special Administrative Region of China
  • T.T. Lam
    Ophthalmology & Visual Science, Chinese Univ Hong Kong, Hong Kong, Hong Kong Special Administrative Region of China
    Doheny Eye Institute, Univ Southern California, Los Angeles, CA
  • J. Caprioli
    Jules Stein Eye Institute, Univ California Los Angeles, Los Angeles, CA
  • Footnotes
    Commercial Relationships  J.M. Kwong, None; K. Chiu, None; W.W.Y. Li, None; T.T. Lam, None; J. Caprioli, None.
  • Footnotes
    Support  Direct grant, CUHK, Hong Kong and RPB
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 161. doi:
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      J.M. Kwong, K. Chiu, W.W. Y. Li, T.T. Lam, J. Caprioli; Calpain and N–Methyl–D–Aspartate (NMDA)–Induced Excitotoxicity in Rat Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):161.

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

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Abstract

Abstract: : Purpose: To examine the involvement of µ– and m–calpain in N–methyl–D–aspartate (NMDA)–induced excitotoxicity in the adult rat retina. Methods: Forty–five to fifty–five day–old albino Sprague Dawley rats were given intravitreal injections of 8 nmoles NMDA. Animals were euthanized at 1, 3, 6, 9, 12, 18 or 24 hours after injection. Immunohistochemistry and Western blotting of µ– and m–calpain were performed on retinas. Colocalization studies of TdT–mediated biotin–dUTP nick end labeling (TUNEL) and µ– or m–caplain immunoreacticity were conducted on retinal sections from animals 12 hours after NMDA injection. The effect of a calpain inhibitor on NMDA–induced excitotoxicity was evaluated by counting retinal ganglion cell (RGC)–like cells 7 days after injection and counting TUNEL positive cells 18 hours after injection. Results: Increased immunoreactivity of µ–calpain was noted in cells at the RGC layer and inner nuclear layer with a maximal expression at 12 hours after NMDA injection. This was confirmed by Western blotting. TUNEL positive cells in the inner retina colocalized with moderate or intense µ–calpain immunoreactivity. In contrast, there was no remarkable change in m–calpain immunoreactivity at all time points after NMDA injection. Simultaneous injection of 2 nmoles of a calpain inhibitor (calpain inhibitor II) significantly reduced the number of TUNEL positive cells in the inner retina (P=0.01, 98% in RGC layer; P=0.04, 97% in inner nuclear layer) 18 hours after NMDA injection, and preserved RGC–like cells counted in central retina (P=0.01, 89%) and peripheral retina (P=0.02, 100%) 7 days after injection. Conclusions: µ–Calpain may be involved in mediating NMDA–induced excitotoxicity in retinas and calpain inhibitors may play a therapeutic role in NMDA related diseases.

Keywords: neuroprotection • ganglion cells • apoptosis/cell death 
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