CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
LEUKOCYTE AS KEY PLAYERS IN OPTIC NERVE DAMAGE INDUCED BY OPTIC NEURITIS
Autor/es:
GONZÁLEZ FLEITAS MF; DORFMAN D; GUERRIERI D; ROSENSTEIN RE; DEVOUASSOUX JD; SANDE PH; ARANDA ML
Lugar:
Buenos Aires
Reunión:
Congreso; Joint meeting of bioscience societies; 2017
Resumen:
Optic neuritis (ON) is a condition involving primary inflammation,demyelination, and axonal injury in the optic nerve which leads to retinalganglion cell (RGC) loss, and visual dysfunction characterizedby a decrease in pupil light reflex (PLR) and visual evoked 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 characterizedby disruption of the blood-brain barrier (BBB) and increasedleukocyte infiltration. The aim of the present work was to analyze theinvolvement of cell infiltration on visual damage induced by experimentalON. LPS or vehicle were injected into the optic nerve fromadult male Wistar rats. BBB integrity was analyzed through Evansblue perfusion and by using WT-GFPþ/WT chimeric rats. At 6 h post-LPS injection an increase in albumin-Evan?s blue leakage and an increasein optic nerve cellularity was observed. At 24 h post-injection,e-GFP(+) cells (likely macrophages and neutrophils) were identify inLPS-injected optic nerves. Experimental ON induced an increase inthe chemokine CCL2-immunoreactivity (p< 0.01). The injection ofBindarit (a CCL2 inhibitor),as well as the irradiation of animals witha leadshield in their heads,significantly prevented the effect of ONon the PLR(p< 0.01),VEP amplitude (p< 0.01),and RGC number(p