Development of a New Experimental Model of Primary Optic Neuritis

ARANDA ML; DORFMAN D; SANDE PH; ROSENSTEIN RE

Mar del Plata

Congreso; XXX-SAN-Annual-Meeting; 2015

Sociedad Argentina de Investigación en Neurociencias

Sensory SystemsP226.-Development ofaA New Experimental Model of Primary OpticNeuritisMarcos L. Aranda, Damián Dorman, Pablo H. Sande, Ruth E. RosensteinLaboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Facultad de Medicina, CEFyBO,UBA/CONICETmarcos8877@gmail.com_____________________________________________________________Optic neuritis (ON) involves inflammation, demyelination, axonal injury in the optic nerve,retinal ganglion cell (RGC) loss, and visual dysfunction. We investigated the ability of asingle injection of bacterial lipopolysaccharide (LPS) directly into the optic nerve to inducefunctional and structural alterations compatible with ON. For this purpose, optic nervesfrom male Wistar rats were injected with vehicle or LPS. At several time points postinjection,we analyzed: i) visual pathway function (visual evoked potentials (VEPs), ii)anterograde transport from the retina to its projection areas, iii) consensual pupil lightreflex (PLR), iv) optic nerve structure, v) microglia/macrophage (by Iba-1- and ED1-immunostaining), vi) astrocytes (by glial fibrillary acid protein-immunostaining), vii) axonnumber (by toluidine blue staining), vii) demyelination (by myelin basic proteinimmunoreactivity and luxol fast blue staining), viii) optic nerve ultrastructure, and ix) RGCnumber (by Brn3a immunoreactivity). LPS induced a significant and persistent decrease inVEP amplitude and PLR, a deficit in anterograde transport, and an early inflammatoryresponse consisting in an increased cellularity, and Iba-1 and ED1-immunoreactivity in theoptic nerve, which were followed by changes in axonal density, astrocytosis,demyelination, and axon and RGC loss. These results suggest that the microinjection of LPSinto the optic nerve may serve as a new experimental model of primary ON.