Abstract

Aims/Purpose: Recently investigations have shown that using sodium iodate (NaIO3) provides a promising animal model of retinal neurodegeneration. The aim of this research is to characterize the effects of this compound in the visual pathway.Methods: First, a single dose of NaIO3 (65 mg/kg) was administered intraperitoneally to mice (C57BL/6J strain) with a knock‐out mutation for the Opn4 gene (Opn4−/−). Then, behavioural tests (light avoidance assay, optomotor test, pupillary light reflex) were performed until Day 28. Electrophysiological tests (electroretinogram, ERG; visual evoked potentials, VEP), were performed weekly until Day 42. Finally, the retina was analysed histologically by immunohistochemical methods on day 57th.Results: First, the results of the behavioural test in the experimental group (NaIO3) reflected a progressive decrease in light sensitivity after 28 days, and a decrease in visual acuity and as well as a completely loss of the pupillary light reflex after 7 days since the administration. Second, the electrophysiological activity of retina and primary visual cortex (ERG, VEP) was significantly reduced in the treated group (NaIO3) with respect to the control group. Finally, histological analysis of the retina showed structural alterations in the outer segments of the photoreceptors of the treated animals (NaIO3).Conclusions: This research demonstrates the appearance of alterations in the outer retina and a decrease in the response at the level of the visual cortex after NaIO3 administration, as expected. This confirms that NaIO3‐induced retinal neurodegeneration is effective in obtaining a promising experimental model that could be used in the study of diseases associated with the visual system and in the development of novel therapeutic strategies.

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