Artikel
Is there endogenous neuroprotection in the retina?
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Autoren
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R. Rejdak
- Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University of Lublin, Poland
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F. Schuettauf
- University Eye Hospital Tuebingen, Germany
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S. Thaler
- University Eye Hospital Tuebingen, Germany
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T. Zarnowski
- Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University of Lublin, Poland
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Z. Zagorski
- Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University of Lublin, Poland
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W. Turski
- Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University of Lublin, Poland
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E. Zrenner
- University Eye Hospital Tuebingen, Germany
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A. Juenemann
- Department of Ophthalmology, University of Erlangen-Nuerenberg, Germany
| Veröffentlicht: | 18. September 2006 |
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Gliederung
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Aspects of endogenous neuroprotective mechanism are still discussed. Kynurenine aminotransferases (KATs I and II) are pivotal to the synthesis of kynurenic acid (KYNA), the only known endogenous glutamate receptor antagonist and neuroprotectant. Our studies revealed presence of KATs in the avian, rodent and human retina documenting expression of KAT I in Müller cell endfeet and KAT II in retinal ganglion cells. Moreover, developmental changes of KATs expression and KYNA concentrations were also documented in the avian and rodent retina.
Studies using various animal models of retinal neurodegeneration showed alterations of KYNA synthesis in the retina in response to retinal ganglion cell damage induced with NMDA and homocysteine intravitreal injections. Interestingly, we also documented age-dependent decrease of retinal KYNA and kynurenine aminotransferases in DBA/2J mice, a model of ocular hypertension.
Only recently, we have shown presence of KAT I and II immunoreactivity in corpora amylacea (CAm) and drusen occurring in human retina as a hallmark of ageing and degeneration. Expression of KATs in CAm and drusen in the human retina suggest that both enzymes may be involved in mechanisms of retinal ageing and neurodegeneration leading to CAm and drusen formation.
We hypothesise that alterations of KYNA formation might be a mechanism of retinal ageing and degeneration. Further studies on pharmacological modulation of this metabolic pathway as a strategy against neurodegenerative diseases of the retina are indicated.
