Programmed cell death of retinal ganglion cells during experimental glaucoma

“…These models rely on obstruction of the outflow pathways by several methods either at the TM (Morrison 1997;Ueda 1998;Levkovitch-Verbin 2002) or more distally (Garcia-Valenzuela 1995). The effect of IOP elevation on RGCs is determined by counting either their soma or their optic nerve (ON) axons and comparison with the contralateral control eye in each animal at the conclusion of the experiment.…”

Section: Introductionmentioning

confidence: 99%

“…In an effort to quantify accurately the location and extent of damage associated with elevated IOP in the first-reported rat model of experimental glaucoma, that is induced by episcleral vein cauterization (Garcia-Valenzuela 1995), we have applied a method we have developed for sampling-independent counting of retrograde dye-labeled RGCs in flat-mounts of the rat retina (Danias 2002). This method can additionally provide information on the spatial geometry and relative size distribution of RGCs.…”

Section: Introductionmentioning

confidence: 99%

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Danias

Shen

Kavalarakis

et al. 2006

Experimental Eye Research

View full text Add to dashboard Cite

Episcleral vein cauterization (EVC) is used in rats to generate a glaucoma model with high intraocular pressure (IOP). The long-term retinal damage in this glaucoma model however, has not been accurately quantified. We report the location and amount of retinal ganglion cell (RGC) damage caused by (EVC) induced IOP elevation in two rat strains.IOP was raised in one eye of Wistar(N=5) and Brown-Norway(B-N)(N=7) rats by EVC and monitored monthly until IOP in contralateral eyes equalized at 5 months post-surgery. Animals were maintained for 3.5-4.5 additional months. B-N rats(N=7) that had no EVC served as controls for this strain. Scotopic flash ERGs were recorded at baseline and just prior to euthanasia. Automated counts of all retrogradely labeled RGCs in retinal flat-mounts were determined and compared between contralateral eyes. RGC density maps were constructed and RGC size distribution was determined.Oscillatory potentials in the group of eyes which had elevated IOP were decreased at the time of euthanasia, when IOP had returned to normal. A group of normal B-N rats had similar RGC counts between contralateral eyes. In the experimental group the mean number of RGCs was not significantly different between control and experimental eyes, but 1 of 5 Wistar and 2 of 7 B-N experimental eyes had at least 30% fewer RGCs from contralateral control eyes. Total retinal area in B-N experimental eyes was higher compared with contralateral eyes. Cumulative IOP exposure of the experimental eyes was modestly correlated with RGC loss while oscillatory potentials appeared to be inversely related to RGC loss. In retinas with extensive (>30% RGC loss) but not complete damage, smaller cells were preserved better than larger ones.The above results indicate that RGC loss in both Wistar and B-N strains is variable after a prolonged elevation of IOP via EVC. Such variability despite equivalent IOP levels and ERG abnormalities, suggests unknown factors that can protect IOP-stressed RGCs. Identification and enhancement of such factors could prove useful for glaucoma therapy.

show abstract

“…La primera fase, influenciada por el principal factor de riesgo (la hipertensión intraocular), induce una alteración del correcto trofismo de las células ganglionares de la retina. Según las teorías mecánica y vascular, el aumento de la presión intraocular estimula una cadena de eventos que induce la apoptosis de las células ganglionares de la retina 8 . La producción de radicales libres, así como la neurotoxicidad del óxido nítrico y la excitotoxicidad mediada por el glutamato amplifican los efectos iniciales de la lesión, favoreciendo el avance y la progresión del glaucoma 9 .…”

Section: Glaucomaunclassified

Aplicaciones de los cannabinoides en glaucoma

Pinar-Sueiro

Rodrı́guez-Puertas

Vecino

2011

Archivos de la Sociedad Española de Oftalmología

View full text Add to dashboard Cite

Introducción: El glaucoma es una neuropatía óptica lentamente progresiva que constituye una de las principales causas de ceguera legal en el mundo. Actualmente existe un limitado grupo de fármacos tópicos para su manejo médico, siendo necesario enfocar la investigación hacia nuevos horizontes terapéuticos como el potencialmente útil grupo de los agonistas de cannabinoides.Objetivo: Revisar a través de la literatura científica actual, los efectos beneficiosos a través de distintas vías de administración de los cannabinoides para la neuropatía óptica glaucomatosa.Desarrollo: Los receptores de cannabinoides han demostrado una amplia expresión en los tejidos oculares implicados en la regulación de la tensión ocular, así como en las capas internas de la retina. Mediante la activación de receptores específicos CB1, CB2 y vías aún no bien conocidas, los agonistas de cannabinoides han demostrado un claro efecto hipotensor ocular, así como un probado efecto neuroprotector sobre las células ganglionares de la retina en estudios experimentales.Conclusiones: Algunos cannabinoides (WIN 55212-2, anandamida) han demostrado a nivel experimental actuar como «fármacos ideales» en el manejo del glaucoma, al presentar buena tolerancia tras su aplicación tópica, reducir de forma eficaz la presión intraocular, y presentar un probado carácter neuroprotector sobre las células ganglionares de la retina.Se deben realizar más estudios sobre su seguridad y ensayos clínicos para poder examinar la utilidad de estos fármacos en el tratamiento del glaucoma en nuestra clínica diaria.

show abstract

Programmed cell death of retinal ganglion cells during experimental glaucoma

Cited by 402 publications

References 3 publications

Animal models of optic nerve diseases

Animal models of optic nerve diseases

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Aplicaciones de los cannabinoides en glaucoma

Contact Info

Product

Resources

About