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1 General aspects (0)   1.1 Epidemiology (4)   1.2 Population genetics (1)   1.3 Pathogenesis (4)   1.4 Quality of life (2)   1.5 Glaucomas as cause of blindness (6)   1.6 Prevention and screening (4) 2 Anatomical structures in glaucoma (1)   2.1 Conjunctiva (0)   2.2 Cornea (6)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (2)     2.5.1 Trabecular meshwork (5)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (0)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (2)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (0)   2.13 Retina and retinal nerve fibre layer (13)   2.14 Optic disc (6)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (1)   3.1 Microscopy (1)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (7)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (10)     3.4.2 Gene studies (1)   3.5 Molecular biology incl. SiRNA (11)   3.6 Cellular biology (5)   3.7 Biochemistry (2)   3.8 Pharmacology (3)   3.9 Pathophysiology (2)   3.10 Immunobiology (0)   3.11 Pharmacogenetics (0)   3.12 Proteomics (0)   3.13 In vivo imaging (0)     3.13.1 Laser Scanning (0)       3.13.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       3.13.1.2 Confocal Scanning Laser Polarimetry (0)     3.13.2 Optical Coherence Tomography (0)       3.13.2.1 Anterior Segment (0)       3.13.2.2 Posterior Segment (0)     3.13.3 RGC Imaging (0)     3.13.4 Other (0)   3.20 Other (2) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (24)   5.1 Rodent (0)   5.2 Primates (0)   5.3 Other (0) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (18)     6.1.1 Devices, techniques (0)     6.1.2 Fluctuation, circadian rhythms (0)     6.1.3 Factors affecting IOP (0)   6.2 Tonography, aqueous flow measurement (see also 2.6) (1)   6.3 Biomicroscopy (slitlamp) (2)     6.3.1 Anterior segment (1)     6.3.2 Posterior segment (0)   6.4 Gonioscopy (1)   6.5 Ophthalmoscopy (0)   6.6 Visual field examination and other visual function tests (0)     6.6.1 Conventional manual (0)     6.6.2 Automated (4)     6.6.3 Special methods (e.g. color, contrast, SWAP etc.) (9)   6.7 Electro-ophthalmodiagnosis (5)   6.8 Photography (0)     6.8.1 Anterior segment (0)     6.8.2 Posterior segment (3)   6.9 Computerized image analysis (0)     6.9.1 Laser scanning (13)       6.9.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       6.9.1.2 Confocal Scanning Laser Polarimetry (0)     6.9.2 Optical coherence tomography (9)       6.9.2.1 Anterior (0)       6.9.2.2 Posterior (0)     6.9.5 Other (1)   6.10 Fluorescein (ICG) angiography (0)     6.10.1 Anterior segment (0)     6.10.2 Posterior segment (0)   6.11 Bloodflow measurements (4)   6.12 Ultrasonography and ultrasound biomicroscopy (1)   6.13 Provocative tests (1)   6.19 Telemedicine (1)   6.20 Progression (6)   6.30 Other (2) 8 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with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (0)       9.4.11.2 Glaucomas in aphakia and pseudophakia (0)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (0)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (0)     9.4.15 Glaucoma in relation to systemic disease (3)     9.4.20 Other (0) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (2) 11 Medical treatment (0)   11.1 General management, indication (4)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (1)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (2)     11.3.4 Betablocker (10)     11.3.5 Other (0)   11.4 Prostaglandins (15)   11.5 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tube implant (10)     12.8.2 With tube implant or other drainage devices (9)     12.8.3 Non-perforating (3)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (8)     12.8.11 Complications, endophthalmitis (3)   12.9 Trabeculotomy, goniotomy (1)   12.10 Cyclodestruction (2)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (1)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (9)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (2)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (1)   12.20 Other (1) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (7) 15 Miscellaneous (7)

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Abstract #13521 Published in IGR 8-1

Assessment of neuroprotective effects of glutamate modulation on glaucoma-related retinal ganglion cell apoptosis in vivo

Guo L; Salt TE; Maass A; Luong V; Moss SE; Fitzke FW; Cordeiro MF
Investigative Ophthalmology and Visual Science 2006; 47: 626-633

See also comment(s) by Makoto Araie •

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PURPOSE: To assess the neuroprotective effects of different glutamate modulation strategies, with a nonselective (MK801) and a selective (ifenprodil) NMDA receptor antagonist and a metabotropic glutamate receptor agonist (mGluR Group II, LY354740), in glaucoma-related in vivo rat models of retinal ganglion cell (RGC) apoptosis. METHODS: RGC apoptosis was induced in Dark Agouti (DA) rats by staurosporine (SSP) treatment. Single agents MK801, ifenprodil, or LY354740, or MK801 and LY354740 combined, were administrated intravitreally at different doses. Eyes were imaged in vivo using a recently established technique and the results confirmed histologically. The most effective combined therapy regimen of MK801 and LY354740 was then assessed in a chronic ocular hypertension (OHT) rat model with application at 0, 1, and 2 weeks after OHT surgery and the effects assessed as described before. RESULTS: All strategies of glutamate modulation reduced SSP-induced-RGC apoptosis compared with the control, in a dose-dependent manner: MK801 (R² = 0.8863), ifenprodil (R² = 0.4587), and LY354740 (R² = 0.9094), with EC50s of 0.074, 0.0138, and 19 nanomoles, respectively. The most effective combination dose of MK801 and LY354740 was 0.06 and 20 nanomoles (P < 0.05), respectively, and the optimal timing of the therapy was 0 weeks after OHT surgery (P < 0.05). CONCLUSIONS: This novel SSP model was validated as a useful tool for screening neuroprotective strategies in vivo. Group II mGluR modulation may be a useful treatment for RGC death. Combination therapy optimized to limit neurotoxic effects of MK801 may be an effective neuroprotective approach in retinal degenerative disease. Furthermore, treatments that minimize secondary RGC degeneration may be most useful in glaucoma.

Dr. L. Guo, Glaucoma and Optic Nerve Head Research Group, Department of Pathology, University College London Institute of Opthamology, London, UK

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Classification:

11.8 Neuroprotection (Part of: 11 Medical treatment)
2.13 Retina and retinal nerve fibre layer (Part of: 2 Anatomical structures in glaucoma)
5 Experimental glaucoma; animal models

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