CONICET | Buscador de Institutos y Recursos Humanos

Optic neuritis (ON) isa condition involving primary inflammation, demyelination, and axonal injury inthe optic nerve which leads to retinal ganglion cell (RGC) loss, and visualdysfunction characterized by a decrease in pupil light reflex (PLR) and visualevoked potentials (VEPs).We have developed an experimental model of primary ONin rats through a single microinjection of bacterial lipopolysaccharide (LPS)into the optic nerve.Neuroinflammatory diseases are characterized by disruptionof the blood-brain barrier (BBB) and increased leukocyte infiltration. The aimof the present work was to analyze the involvement of cell infiltration onvisual damage induced by experimental ON. LPS or vehicle were injected into theoptic nerve from adult male Wistar rats. BBB integrity was analyzed throughEvans blue perfusion and by using WT-GFPþ/WT chimeric rats. At 6 h post-LPSinjection an increase in albumin-Evan's blue leakage and an increase in opticnerve cellularity was observed. At 24 h post-injection, e-GFP(+) cells (likelymacrophages and neutrophils) were identify in LPS-injected optic nerves.Experimental ON induced an increase in the chemokine CCL2-immunoreactivity (p< 0.01). The injection of Bindarit (aCCL2 inhibitor),as well as the irradiation of animals with a leadshield intheir heads,significantly prevented the effect of ON on the PLR(p< 0.01),VEP amplitude (p< 0.01),and RGC number(p< 0.01).These results indicate thatleukocyte recruitment plays a key role in the visual damage induced byexperimental ON.