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Hana Levkovitch–Verbin, Cathy Harris–Cerruti, Yoram Groner, Larry A. Wheeler, Michal Schwartz, Eti Yoles; RGC Death in Mice after Optic Nerve Crush Injury: Oxidative Stress and Neuroprotection. Invest. Ophthalmol. Vis. Sci. 2000;41(13):4169-4174.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To establish a method for morphometric analysis of retrogradely labeled
retinal ganglion cells (RGCs) of the mouse retina, to be used for the
study of molecular aspects of RGC survival and neuroprotection in this
model; to evaluate the effect of overexpression of Cu-Zn-superoxide
dismutase (CuZnSOD) on RGC survival after severe crush injury to the
optic nerve, and to assess the effect of the α2-adrenoreceptor
agonist brimonidine, recently shown to be neuroprotective, on RGC
methods. A severe crush injury was inflicted unilaterally in the orbital portion
of the optic nerves of wild-type and transgenic (Tg–SOD) mice
expressing three to four times more human CuZnSOD than the wild type.
In each mouse all RGCs were labeled 72 hours before crush injury by
stereotactic injection of the neurotracer dye FluoroGold (Fluorochrome,
Denver, CO) into the superior colliculus. Survival of RGCs was then
assessed morphometrically, with and without systemic injection of
results. Two weeks after crush injury, the number of surviving RGCs was
significantly lower in the Tg−SOD mice (596.6 ± 71.9
cells/mm2) than in the wild-type control mice (863.5 ± 68 cells/mm2). There was no difference between the
numbers of surviving RGCs in the uninjured retinas of the two strains
(3708 ± 231.3 cells/mm2 and 3904 ± 120
cells/mm2, respectively). Systemic injections of
brimonidine significantly reduced cell death in the Tg−SOD mice, but
not in the wild type.
conclusions. Overexpression of CuZnSOD accelerates RGC death after optic nerve
injury in mice. Activation of the α2-adrenoreceptor pathway by
brimonidine enhances survival of RGCs in an in vivo transgenic model of
excessive oxidative stress.
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