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Yong H. Park, Hidehiro Oku, Masahiro Fukuhara, Takuji Kurimoto, Tsunehiko Ikeda, Thomas Yorio, Adnan Dibas; Ocular GluR1 And GluR2 Expression Following Retinal Injury. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5343.
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© ARVO (1962-2015); The Authors (2016-present)
Changes in the expression of AMPA receptors subunits (GluR1-4) have been reported in a number of diseases. However, such changes and mechanisms remain to be evaluated for retinal injury after optic nerve crush. This study was designed to analyze changes in the expression of GluR1 and GluR2 following optic nerve crush.
The optic nerve of the right eye of Wistar rats was crushed. Retinal ganglion cells (RGCs) were retrogradely labeled by applying fluorogold onto the left superior colliculus one week prior to crushing. Retinal injuries were induced by optic nerve crush in rat eyes. Real-time PCR (qPCR) was used for measuring changes in GluR1, GluR2, and β-actin messages. Changes in glial fibrillary acidic protein (GFAP) and GluRs expression were also followed in total retinal extracts using western blotting.
The mean number (±SD) of RGCs labeled retrogradely from superior colliculus was 2089.6 ± 85.2/mm2 in rats without any treatment, which decreased to 1090.8 ± 77.6 (52.2%) and 496.6 ± 87.3/mm2 (23.7%) on day 7 and 14, respectively. GluR1 and GluR2 mRNA levels were decreased at 7 and 14 days. While GFAP (a marker of astrogliosis) increased at 2, 7 and 14 days, GluR2 decreased significantly at 7 and 14 days (by 30%) as determined by western blotting. Interestingly, glutamine synthetase initially increased at 2 days, but decreased at 7 and 14 days post optic nerve crush as determined by western blotting.
The reduced expression of GluR1 and GluR2 suggest dysfunctional ion coupling in retina following optic nerve crush and likely impaired retinal function. The increased GFAP suggests astrogliosis while the changes in glutamine synthetase indicate abnormalities in Muller cells function. Further studies are needed to identify the site of GluR1 and GluR2 changes and to characterize the mechanism involved in down regulation of the glutamate receptors.
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