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Retinal neuronal death caused by ocular hypertension
Author(s) -
VIDALSANZ M,
SALINASNAVARRO M,
VALIENTESORIANO FJ,
ORTíNMARTíNEZ A,
NADALNICOLáS FM,
ALARCóNMARTíNEZ L,
AVILéSTRIGUEROS M,
AGUDOBARRIUSO M,
VILLEGASPéREZ MP
Publication year - 2012
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2012.3233.x
Subject(s) - retina , retinal , axotomy , ocular hypertension , optic nerve , axoplasmic transport , ophthalmology , ischemia , anatomy , medicine , retinal ganglion cell , ganglion cell layer , population , biology , neuroscience , intraocular pressure , central nervous system , environmental health
Purpose To characterize the anatomical and functional changes that follow ocular hypertension (OHT). Methods In adult albino rats or mice, the episcleral and perilimbar veins were photocauterized with laser diode. This resulted in OHT that reaches basal levels by one week in mice and by three weeks in rats. Results OHT induces anatomical and functional degenerative retinal changes. One week after lasering there is impairment of the retrograde axonal transport which is first functional and then mechanic. By two weeks there is loss of approximately 80% of the RGC population without further progression. RGCs loss occurs mainly in pie‐shaped sectors but is also diffuse throughout the retina. The intraretinal RGC axons and somas show signs compatible with a slow retrograde axonal degeneration resembling an optic nerve crush. OHT induces loss of RGCs but not of other non RGC neurons present in the ganglion cell layer, namely the displaced amacrine cells, for periods of up to six months after OHT. There is a protracted and progressive affectation of the outer retina which results in a major loss of LM‐ and S‐cones. This anatomical data are supported by functional analyses. Electroretinogram recordings show maintained and significant diminutions of the scotopic threshold responses as well as of the a‐ and b‐waves indicating permanent alterations of the inner and outer retinal layers, respectively. Conclusion OHT results both in RGC axonal crush‐like injury and in an ischemic damage to the outer retinal layers. Thus, this model may be used to study axotomy‐ or ischemia‐induced neuronal death in the innermost retina or in the outer retina, respectively.