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E. R. Ritchey, M. A. Scott, A. J. Fischer; FGF2, Müller Glia and Neuroprotection in the Chicken Retina. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2075. doi: https://doi.org/.
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Current research in neuroprotection and the retina has focused on improving the resistance of neurons to damage. To date, the role of improving the neuroprotective properties of Müller glia is poorly understood. We examine the role of FGF2 on Müller glia and neuroprotection in the chicken retina.
White leghorn chickens received intravitreal injections of either 0.2µg of FGF2, 1µg insulin, FGF2+insulin or the MAP Kinase inhibitor UO126 on postnatal days 5 and 6. On postnatal day 7, all eyes received 1µg NMDA treatment. At postnatal day 8, all eyes received BrdU and were sacrificed 4 hours after injection. Retinas were fixed, sectioned and labeled for TUNEL, BrdU, PCNA, cFos, Egr1 and pCREB.
In response to FGF2 treatment, levels of cFos and pCREB increase in Müller glia. Similarly, treatment with insulin increases levels of cFos and pCREB as well Egr1 in the Müller glia. FGF2 prior to NMDA treatment caused a significant reduction in the number of TUNEL positive cells in the Inner Nuclear Layer (INL). Insulin prior to NMDA treatment caused a significant increase in the number of TUNEL positive cells in the INL. Treatment with FGF2 + insulin showed no decrease in the number of TUNEL positive cells compared to insulin treatment alone. Treatment with UO126 prior to NMDA produced a significant reduction in TUNEL positive cells in the INL. BrdU and PCNA labeling is increased in the Müller glia in peripheral retina with FGF2 treatment compared to control retinas, where it is not increased in central retina.
The upregulation of cFos and pCREB selectively in Müller glia indicates that the neuroprotective effects of FGF2 may be mediated through the activity of Müller glia. Upregulation of Egr1 in insulin treated eyes, but not in FGF2 treated eyes, suggests that Egr1 may be associated with a loss of neuroprotective capacity. The reduction in TUNEL positive cells resulting from UO126 treatment suggests that FGF2-independent MAP Kinase signaling may normally protect inner retinal neurons from excitotoxicity.
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