CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Neuroprotective effect of melatonin on a neuroinflammation model of the visual pathway
Autor/es:
GONZÁLEZ FLEITAS MF; CHIANELLI MS; ROSENSTEIN RE; DIEGUEZ HH; SANDE PH; ARANDA ML; KELLER SARMIENTO MI; DORFMAN D
Lugar:
CABA
Reunión:
Congreso; 2nd Congress of the Federation of Latin-American and Caribbean Societies for Neuroscience (FALAN); 2016
Institución organizadora:
Societies For Neuroscience
Resumen:
S1P200. Neuroprotective effect of melatonin on a neuroinflammation modelof the visual pathwayMarcos L. Aranda1*, María F. González Fleitas1, Hernàn H. Dieguez1, Maria I. Keller Sarmiento1, Mónica S. Chianelli1, Pablo H. Sande1, Damián Dorfman1, Ruth E. Rosenstein11 Centro de Estudios Farmacológicos y Botánicos, UBA /CONICET*marcos8877@gmail.comWe have developed a new experimental model of optic neuritis (ON) through the microinjection of bacteriallipopolysaccharide (LPS) into the optic nerve, which reproduces central features of human ON. The aim of thiswork was to analyze the effect of melatonin (MEL) on the optic nerve axoglial alterations induced by experimental ON. LPS was injected in one optic nerve from Wistar rats, while the contralateral optic nerve was injected with vehicle. One group of animals received a pellet of MEL one day before LPS or vehicle injection, and another group was submitted to a sham procedure. In another set of experiments, the pellet of melatonin was implanted at 4 days post-injection of LPS or vehicle. The effect of melatonin was analyzed at 21 days post-injection in terms of: i) visual pathway function (visual evoked potentials (VEPs)), ii) anterograde transport, iii) pupil light reflex (PLR), iv) microglia/macrophages v) astrocytes vi) axon number vii) demyelination, viii) retinal ganglion cells (RGCs) number and iv) optic nerve lipid peroxidation (TBARS). LPS induced a significant decrease in VEP amplitude and PLR, a reduction in retinal anterograde transport, an increase in Iba-1 and ED1 immunoreactivity, astrocytosis, demyelization, an increase in lipid peroxidation, and RGC loss. The pre-treatment with MEL prevented all these alterations. The post-treatment with MEL preserved VEP amplitude and PLR. The treatment with melatonin prevented functional and histological alterations probably through an antioxidant mechanism. These results indicate that melatonin could be a promissory resource in the management of ON.