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Akira Takamiya, Youngseok Song, Akitoshi Yoshida; N-methyl-d-aspartate (NMDA)-induced Excitotoxicity After Gliotoxin Treatment In Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2018.
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It is well known that gliotoxin-alpha amino-adipic acid (AAA), which is the glutamate analogue, selectively enters astroglial cells and causes gliotoxicity for the Muller glial cells and astrocytes in the retina. To determine whether the treatment of AAA leads to suppress retinal neuronal cell death by inhibition of the astroglial activity, adult wild type (WT) mice were examined in an experimental model of excitotoxic neural damage.
Retinal neural damage was induced in adult WT mice by intravitreal injection of N-methyl-D-aspartate (NMDA) (50 nmol) 2 days after gliotoxin or PBS treatment. Retinal cell death was determined by TDT-mediated-dUTP nick end labeling (TUNEL) at day 1 after NMDA treatment. At day 7 after the treatment, survival retinal ganglion cells were immunostained with a primary antibody against a ganglion cell specific marker, beta-III tubulin and the number of cells was counted.
At day 1 after NMDA treatment (at day 3 after AAA or PBS treatment), more TUNEL+ cells were counted from retinal sections of PBS pretreated mice than that of AAA treated mice. There were few TUNEL+ cells in AAA or PBS treatment alone. At day 7 after NMDA treatment, more ganglion cells survived in the retinas of AAA treated mice than that in PBS treated mice.
Our results suggest that AAA treatment may induce to protect the retinal neuronal cells from excitotoxic neural injury by inhibition of the activity of Muller glial cells and astroglial cells.
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