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P38 mitogen-activated protein kinase is involved in NMDA-induced retinal ganglion cell death in vivo


, : P38 mitogen-activated protein kinase is involved in NMDA-induced retinal ganglion cell death in vivo. Society for Neuroscience Abstracts 27(1): 697

Glutamate receptor-mediated neurotoxicity is thought to be important in the pathogenesis of a variety of neurodegenerative disorders, including ocular diseases such as glaucoma, ischemia and optic neuropathy. We studied the possible involvement of p38 mitogen-activated protein kinase (MAPK) in NMDA-induced neuronal death in the rat retina in vivo. We injected 200 nmol NMDA and 10 nmol glycine into the vitreous of male Long-Evans rats weighing 200-250 gm. Additionally, in some eyes, we injected several different concentrations of SB203580, a relatively specific inhibitor of p38. For quantitative analysis of survival, we retrogradely labeled the retinal ganglion cells (RGCs) by injecting fluorogold into the superior colliculus 4 days prior to the intravitreal injections. We then counted surviving RGCs 7 days after the intravitreal injections. Immunoblotting and immunohistochemistry using an antibody specific for phosphorylated/activated p38 was performed 1, 3, 6, 12, 24, 48, 72 and 96 hours after intravitreal injection. Phosphorylated/activated p38 was detected by immunoblot 1-24 hrs after NMDA injection. Cells staining positively for phosphorylated/activated p38 were located in the retinal ganglion cell and inner nuclear layers. NMDA produced 90% loss of RGCs. SB203580 afforded statistically significant protection from this insult. We conclude that the p38 MAPK pathway is, at least in part, involved in NMDA-induced retinal ganglion cell death in vivo.

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