INVESTIGADORES
DORFMAN Damian
congresos y reuniones científicas
Título:
Experimental optic neuritis induced by the microinjection of lipopolysaccharide into the optic nerve
Autor/es:
ARANDA ML; DORFMAN D; SANDE PH; ROSENSTEIN RE
Lugar:
Denver
Reunión:
Congreso; ARVO Annual Meeting 2015; 2015
Resumen:
Purpose: Optic neuritis (ON) is a condition involving
primary inflammation, demyelination, and axonal injury in the optic nerve which
leads to retinal ganglion cell (RGC) loss, and visual dysfunction. We
investigated the ability of a single microinjection of bacterial
lipopolysaccharide (LPS) directly into the optic nerve to induce functional and
structural alterations compatible with ON. For this purpose, optic nerves from
male Wistar rats remained intact or
were injected with vehicle or LPS.
Methods: The effect of LPS was evaluated at several
time points post-injection in terms of: i) visual pathway and retinal function
(visual evoked potentials (VEPs) and electroretinograms, (ERGs), respectively),
ii) anterograde transport from the retina to its projection areas, iii) consensual
pupil light reflex (PLR), iv) optic nerve histology, v) microglia/macrophage reactivity
(by Iba-1- and ED1-immunostaining), vi) astrocyte reactivity (by glial
fibrillary acid protein-immunostaining), vii) axon number (by toluidine blue
staining), vii) demyelination (by myelin basic protein immunoreactivity and luxol
fast blue staining), viii) optic nerve ultrastructure, and ix) RGC number (by
Brn3a immunoreactivity).
Results: LPS induced a significant and persistent decrease
in VEP amplitude and PLR,without changes in the ERG. In addition, LPS induced a
deficit in anterograde transport, and an early inflammatory response consisting
in an increased cellularity, and Iba-1 and ED1-immunoreactivity in the optic
nerve, which were followed by changes in axonal density, astrocytosis,
demyelination, and axon and RGC loss.
Conclusions: These results suggest that the
microinjection of LPS into the optic nerve may serve as a new experimental
model of primary ON.