Abstract
Retinal ganglion cell degeneration underlies the pathophysiology of diseases affecting the retina and optic nerve. Several studies have previously evidenced the anti-apoptotic properties of the bile constituent, tauroursodeoxycholic acid, in diverse models of photoreceptor degeneration. The aim of this study was to investigate the effects of systemic administration of tauroursodeoxycholic acid on N-methyl-D-aspartate (NMDA)-induced damage in the rat retina using a functional and morphological approach. Tauroursodeoxycholic acid was administered intraperitoneally before and after intravitreal injection of NMDA. Three days after insult, full-field electroretinograms showed reductions in the amplitudes of the positive and negative-scotopic threshold responses, scotopic a- and b-waves and oscillatory potentials. Quantitative morphological evaluation of whole-mount retinas demonstrated a reduction in the density of retinal ganglion cells. Systemic administration of tauroursodeoxycholic acid attenuated the functional impairment induced by NMDA, which correlated with a higher retinal ganglion cell density. Our findings sustain the efficacy of tauroursodeoxycholic acid administration in vivo, suggesting it would be a good candidate for the pharmacological treatment of degenerative diseases coursing with retinal ganglion cell loss.
Highlights
We used an NMDA-mediated neurotoxicity model combined with a functional and morphological evaluation of the retina to demonstrate a neuroprotective effect of tauroursodeoxycholic acid (TUDCA) on Retinal ganglion cells (RGCs) in vivo
We showed that systemic administration of TUDCA attenuated the functional changes associated with NMDA-induced retinal damage in Sprague-Dawley rats, and delayed RGCs loss
NMDA receptor subunits in the rat retina have been immunohistochemically localized on RGCs and displaced amacrine cells in the ganglion cell layer, as well as in a subset of amacrine cells in the inner nuclear layer [34]
Summary
A twoway repeated measures ANOVA was performed to evaluate the effects of the treatment (vehicle vs TUDCA) on ERG responses throughout the experimental stages (before and after inducing retinal damage with NMDA). To test the neuroprotective effect of TUDCA on retinal function, full-field ERG recording was performed in parallel on a group of rats that received a daily intraperitoneal dose of TUDCA three days prior to NDMA administration, and until their sacrifice (Fig 1A).
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