Death and neuroprotection of retinal ganglion cells after different types of injury
Autor: | S Mayor-Torroglosa, María Paz Villegas-Pérez, M.P. Lafuente, Elena Rodriguez, Inmaculada Sellés-Navarro, Paloma Sobrado-Calvo, Manuel Vidal-Sanz |
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Rok vydání: | 2000 |
Předmět: |
Retina
medicine.medical_specialty genetic structures business.industry General Neuroscience medicine.medical_treatment Ischemia Toxicology medicine.disease Inner plexiform layer Retinal ganglion medicine.anatomical_structure Retinal ganglion cell Anesthesia Ophthalmology Inner nuclear layer medicine Optic nerve sense organs business Ligature |
Zdroj: | Neurotoxicity Research. 2:215-227 |
ISSN: | 1476-3524 1029-8428 |
DOI: | 10.1007/bf03033795 |
Popis: | In adult Sprague-Dawley rats, retinal ganglion cell survival was investigated after intraorbital optic nerve section and after transient ischemia of the retina induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The thickness of the inner nuclear and inner plexiform layers was also assessed after transient periods (120 min) of retinal ischemia induced by selective ligature of the ophthalmic vessels. In addition, we have also investigated the neuroprotective effects of different substances in these paradigms. The intraocular injection of brain-derived neurotrophic factor increased RGC survival after retinal ischemia induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The caspase-inhibitor Z-DEVD increased retinal ganglion cell survival after optic nerve section and also after 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. The peptide Bcl-2 did not increase retinal ganglion cell survival after optic nerve section but increased retinal ganglion cell survival after 60 or 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. Finally, BDNF, nifedipine, naloxone and bcl-2 prevented in part the decrease in thickness of the inner nuclear layer and inner plexiform layer induced by selective ligature of the ophthalmic vessels. Our results suggest that retinal ganglion cell loss induced by different types of injury, may be prevented by substances with neuroprotective effects, by altering steps of the cascade of events leading to cell death. |
Databáze: | OpenAIRE |
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