June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Neuroprotective effect of enriched environment on experimental optic neuritis
Author Affiliations & Notes
  • Marcos Luis Aranda
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Maria Florencia Gonzalez Fleitas
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Hernan Hugo Dieguez
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Maria Ines Keller Sarmiento
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Monica Chianelli
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Pablo Sande
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Damian Dorfman
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Ruth Estela Rosenstein
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships   Marcos Luis Aranda, None; Maria Florencia Gonzalez Fleitas, None; Hernan Hugo Dieguez, None; Maria Ines Keller Sarmiento, None; Monica Chianelli, None; Pablo Sande, None; Damian Dorfman, None; Ruth Rosenstein, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1764. doi:
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      Marcos Luis Aranda, Maria Florencia Gonzalez Fleitas, Hernan Hugo Dieguez, Maria Ines Keller Sarmiento, Monica Chianelli, Pablo Sande, Damian Dorfman, Ruth Estela Rosenstein; Neuroprotective effect of enriched environment on experimental optic neuritis. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1764.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Optic neuritis (ON) is an inflammatory, demyelinating, and neurodegenerative condition of the optic nerve, which might induce permanent vision loss. Enriched environment involves housing conditions which stimulate social interaction, physical, cognitive and explorative activity, and exert beneficial effects on the brain in many central nervous system disorders. However, its therapeutic potential during neuroinflammation remains less understood. The aim of this work was to examine the effect of enriched environment (EE) on optic nerve and retinal damage induced by experimental ON.

Methods : Bacterial lipopolysaccharide (LPS) or vehicle were microinjected into the optic nerve from adult male Wistar rats. Immediately after injections, one group of animals was housed in EE, and another group remained in standard environment (SE) for 21 days.Visual pathway function (visual evoked potentials (VEPs), and pupillary light reflex (PLR)), anterograde transport from the retina to the superior colliculus(after an intravitreal injection of cholera toxin b-subunit),microglial/macrophages reactivity (Iba-1 and ED1-immunoreactivity), astrocytosis (glial fibrillary acidic protein (GFAP) immunohistochemistry), demyelination (luxol fast blue staining), axons (phosphorylated neurofilament heavy immunoreactivity (pNFH) andtoluidine blue staining), retinal ganglion cells (RGC, Brn3a-immunoreactivity), and optic nerve lipid peroxidation (thiobarbituric acid reactive substances) were assessed in vehicle- and LPS-injected optic nerves from animals housed in SE or EE.

Results : EE housing completely prevented the decrease in VEPs and PLR, and anterograde transport induced by experimental ON. In addition, EE prevented the decreased pNFH-immunoreactivity microglia/macrophage reactivity, astrocytosis, demyelination, and axon and RGCloss induced by experimental ON. In SE, LPS-injected optic nerves displayed oxidative damage which was prevented by EE housing. When EE housing started at 4 days post-injection of LPS, a preservation of VEPs and PLR was observed.

Conclusions : These data support that EE housing preserved visual functions and reduced neuroinflammationof the optic nerve.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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