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Evidence for Kynurenic acid (KYNA) Synthesis in the Retina and its Modulation in Response to Retinal Ganglion Cell Loss
1Rejdak R., 2Schüttauf F., 3Zarnowski T., 4Turski W., 5Okuno E., 3Zagórski Z., 2Zrenner E.,
1University Eye Hospital, Department of Pathophysiology of Vision and, Neuroophthalmology (Lublin)
2Eberhard-Karls-Universität Tübingen, Universitäts-Augenklinik, Abt. II, Pathophysiologie des Sehens u. Neuroophthalmologie (Tübingen)
3Lublin University School of Medicine, Tadeusz Krwawicz Chair of Ophthalmology & 1st Eye Hospital (Lublin)
4Lublin University School of Medicine, Department of Pharmacology and Toxicology (Lublin)
5Department of Molecular Medicine (Wakayama)
Background: The tryptophan metabolite kynurenic acid (KYNA) is the only known endogenous glutamate receptor antagonist and neuroprotectant. Only recently, the presence of KYNA and its synthesising enzymes in the inner retina and changes of the retinal KYNA content during ontogeny have been reported (Rejdak et al, NeuroReport, 2001; Rejdak et al., ARVO 2002). The present study is the first to examine modulation of retinal KYNA formation in response to NMDA-induced cell death in adult rat retinal ganglion cells (RGCs).
Methods: Retinae from adult Brown Norway rats were used. Rats were injected with 20-nmol NMDA intraocularly on one eye and 2µl of PBS into contralateral one. To quantify the number of surviving RGCs, the retrograde tracer Fluorogold was injected into the superior colliculi. Surviving RGCs were counted in wholemounts of retinae in a centroperipheral gradient, as well as in the four quadrants, using a computer-assisted image analysis system. Retinal KYNA content was measured 2 and 7 days after NMDA injections. KYNA levels were investigated with HPLC according to the method of Turski et al. (Brain Res 28:164, 1988).
Results: RGC numbers decreased significantly 2 and 7 days after NMDA-injection if compared to control retinae. As determined by HPLC, NMDA-treated eyes displayed a significantly higher retinal KYNA concentration (p=0.03) two days after injections comparing to controls. Importantly, 7 days after injections a significant decrease of KYNA content (p=0.02) was observed in retinae of NMDA-treated eyes.
Conclusions: We have shown that the retinal KYNA content changes in response to NMDA-induced RGCs damage. It is therefore conceivable that KYNA deficiency is causally related to the pathology of excitotoxic retinal diseases. Further evaluation of KYNA role in the pathomechanisms of retinal disorders is recommended and being performed.
Supported by the German Ophthalmologic Society and NATO Individual Research Fellowship