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Currently, there are no effective therapies for this disorder. We have developed an experimental model of primary <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content> in rats through a single microinjection of 4.5 <jats:italic>\u03bc<\/jats:italic>g of bacterial lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>) into the optic nerve. Since melatonin acts as a pleiotropic therapeutic agent in various neurodegenerative diseases, we analyzed the effect of melatonin on <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content>. For this purpose, <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> or vehicle were injected into the optic nerve from adult male <jats:italic>Wistar<\/jats:italic> rats. One group of animals received a subcutaneous pellet of 20 mg melatonin at 24 hr before vehicle or <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> injection, and another group was submitted to a sham procedure. Melatonin completely prevented the decrease in visual evoked potentials (<jats:styled-content style=\"fixed-case\">VEP<\/jats:styled-content>s), and pupil light reflex (<jats:styled-content style=\"fixed-case\">PLR<\/jats:styled-content>), and preserved anterograde transport of cholera toxin <jats:italic>\u03b2<\/jats:italic>\u2010subunit from the retina to the superior colliculus. Moreover, melatonin prevented microglial reactivity (<jats:styled-content style=\"fixed-case\">ED<\/jats:styled-content>1\u2010immunoreactivity, <jats:italic>P<\/jats:italic> &lt; 0.01), astrocytosis (glial fibrillary acid protein\u2010immunostaining, <jats:italic>P<\/jats:italic> &lt; 0.05), demyelination (luxol fast blue staining, <jats:italic>P<\/jats:italic> &lt; 0.01), and axon (toluidine blue staining, <jats:italic>P<\/jats:italic> &lt; 0.01) and retinal ganglion cell (Brn3a\u2010immunoreactivity, <jats:italic>P<\/jats:italic> &lt; 0.01) loss, induced by <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>. Melatonin completely prevented the increase in nitric oxide synthase 2, cyclooxygenase\u20102 levels (Western blot) and <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content><jats:italic>\u03b1<\/jats:italic> levels, and partly prevented lipid peroxidation induced by experimental <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content>. When the pellet of melatonin was implanted at 4 days postinjection of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>, it completely reversed the decrease in <jats:styled-content style=\"fixed-case\">VEP<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">PLR<\/jats:styled-content>. These data suggest that melatonin could be a promising candidate for <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content> treatment.<\/jats:p>","DOI":"10.1111\/jpi.12318","type":"journal-article","created":{"date-parts":[[2016,2,16]],"date-time":"2016-02-16T15:12:42Z","timestamp":1455635562000},"page":"360-372","source":"Crossref","is-referenced-by-count":32,"title":["Neuroprotective effect of melatonin in experimental optic neuritis in rats"],"prefix":"10.1111","volume":"60","author":[{"given":"Marcos L.","family":"Aranda","sequence":"first","affiliation":[{"name":"Laboratory of Retinal Neurochemistry and Experimental Ophthalmology Department of Human Biochemistry School of Medicine\/CEFyBO University of Buenos Aires\/CONICET Buenos Aires Argentina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda F.","family":"Gonz\u00e1lez Fleitas","sequence":"additional","affiliation":[{"name":"Laboratory of Retinal Neurochemistry and Experimental 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