Effect of enriched environment housing on glutamate-induced damage in adult rat retina

DORFMAN D; DIEGO FERNANDEZ; CHIANELLI, MONICA; ARANDA M; ROSENSTEIN R

Seattle

Congreso; The Association For Research In Vision And Ophthalmology (Arvo); 2013

ARVO

Abstract Purpose:Glutamate, the main excitatory neurotransmitter in the retina, is toxic when present in excessive amounts. In fact, glutamate-induced excitotoxicity has been involved in different retinal diseases. The aim of this study was to elucidate whether enriched environment (EE) housing protects the retina from glutamate-induced damage in adult rats. Methods:Adult male Wistar rats were intravitreally injected with a 4 μL of 0.3 M glutamate in one eye and vehicle in the contralateral eye. Immediately after injections, animals were housed in standard laboratory cages (standard environment, (SE)) or EE. EE consisted of big cages containing 6 animals/cage, and several food hoppers, wheels and different objects repositioned once/day and fully substituted once/week. After 1 week of SE or EE housing, retinal function (scotopic electroretinography, ERG), and retinal morphology (optical microscopy) were analyzed. Müller cell glial fibrillary acidic protein (GFAP) levels and Brn3a(+) retinal ganglion cell (RGC) number were assessed by immunohistochemistry. Anterograde transport from the retina to the superior colliculus was examined after an intravitreal injection of cholera toxin β-subunit. Results:In SE-housed (control) animals, glutamate induced a significant decrease in ERG a- and b- wave and oscillatory potential amplitude, whereas EE housing significantly reduced these alterations. In animals exposed to SE, glutamate induced a significant RCG loss, and an increase in Müller cell GFAP levels, which were reversed by EE housing. In control animals, glutamate induced a deficit in the anterograde transport which was preserved by EE housing. Conclusions:These results suggest that EE housing could become a future and novel therapy for retinal diseases which involve glutamate-mediated retinal damage.