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Abstract
SA.08.04
Excitotoxicity in glaucomatous optic nerve degeneration – neuroprotective approaches
Frank Schüttauf
Department für Augenheilkunde, Eberhard-Karls-Universität Tübingen
Recent findings of basic research conclude a leading role of excitotoxicity in the development of glaucomatous optic nerve degeneration. Excitotoxicity is an unphysiologically permanent depolarization due to uncontrolled release of excitatory neurotransmitters while energy is constantly low. An increased concentration of excitatory neurotransmitters, mainly glutamate, was documented in various ischemically or traumatically induced neurological disorders. Yet, the involvement of glutamate in the disease process leading to glaucoma is debatable. Increased concentrations of glutamate lead to activation of different cellular receptors, predominantly of the N-methyl-D-aspartat- (NMDA-) subtype of the glutamate receptor, followed by a release a free radicals and an activation of the nitric oxide (NO) pathway. The origin of the increased glutamate concentration is not fully understood: Retinae of glaucoma patients and in experimental glaucoma showed a reduced expression of glutamate transporters. Additionally the release of glutamate from degenerating retinal ganglion cells (RGC) might be of importance. In parallel, the increased production of nitric oxide finally contributes to glaucomatous RGC death: The concentration of NO synthase is increase in the optic disc of glaucoma patients while an imbalance of NO changes ocular perfusion pressure. While the potential of NMDA receptor blockers has been demonstrated by different research groups in vivo the main challenge remains to balance the protective effect of anti-excitotoxic agents and the suppression of physiological neuronal function. At the same time, the knowledge transfer from animal models to a potential treatment of human glaucoma has been less satisfactory. Therefore, the aim of this presentation to elucidate chances and pitfalls of a potential anti-excitotoxic glaucoma treatment.
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