Exposición al ambiente enriquecido protege las alteraciones de la retina y EPR inducidas por la AMD experimental en ratones

ROMEO, HORACIO E.; IAQUINANDI, AGUSTINA; SANDE PABLO H.; ALAIMO, AGUSTINA; CHIANELLI MÓNICA S; ROSENSTEIN, RUTH E; DIEGUEZ, HERNÁN H.; CALANNI, JUAN S.; KELLER SARMIENTO, MARÍA I.; DORFMAN, DAMIÁN

Formato Virtual

Congreso; XIII Congreso de la Asociación de Investigación en Visión y Oftalmología; 2021

AIVO

Dry age-relatedmacular degeneration (dAMD), the world´s blindness leading cause in theelderly, is characterized by the progressive degeneration of photoreceptors(PR) and retinal pigment epithelium (RPE) circumscribed to the macula.Currently, there are not available therapies to prevent or delay the disease onsetand progression. We have developed an experimental model of AMD throughunilateral superior cervical ganglionectomy (SCGx) in mice, which reproducesthe disease central hallmarks. Environmental enrichment (EE) is a paradigm hasproven neuroprotective effects in the adult retina within experimentalneurodegenerative diseases in rodents. Our aim was to analyze the effect of EEon the outer retina/RPE alterations induced by experimental dAMD. Adult maleC57BL/6j mice were submitted to unilateral SCGx, whereas the contralateral sidewas submitted to a sham procedure and housed either in standard environment(SE) or EE for 10 weeks. Visual function (electroretinography (ERG) and visualbehavior tests) as well as retinal histology were analyzed at 10 weeks post-SCGx.EE prevented the visual dysfunction, the reduction of both RPE melanin contentand RPE65-immunoreactivity, and the RPE/PR ultrastructural alterations inducedby SCGx in SE-housed animals. At 6 weeks post-SCGx, EE prevented oxidativestress, preserved mitochondrial mass and increased BDNF-immunoreactivity at theouter retina and RPE and BDNF protein levels. When EE exposure started at 4weeks post-SGCx, it reversed the functional and histological alterationsinduced by dAMD. In conclusion, the exposure to EE prevented and reversed thealterations induced by experimental dAMD, possibly through oxidative stressmodulation, mitochondria protection and a BDNF-dependent mechanism.