Mynocicline prevents early axoglial alterations of the optic nerve induced by experimental glaucoma.

GONZÁLEZ FLEITAS F.; ALEJANDRA BOSCO; ROSENSTEIN, RUTH E.; PASQUINI, LAURA A.; DAMIÁN DORFMAN; BORDONE, MELINA P.; PABLO SANDE

Ciudad Autónoma de Buenos Aires

Congreso; II Federation of Latin American and Caribbean Neurosciences Societies Congress; 2016

Glaucoma is a leading cause of blindness, characterized by retinal ganglion cell (RGC) loss and optic nerve (ON) damage. Cumulative evidence suggests the participation of glial cells in the degeneration of the ON and RGCs. We analyze the effect of minocycline on early axoglial alterations of the ON in an experimental model of glaucoma induced by chondroitin sulfate (CS) injections into the eye anterior chamber from Wistar rats. A significant decrease in Brn3a(+) RGC number was observed in eyes injected with CS at 10 weeks. A reduction in anterograde transport of B subunit cholera toxin (CTB) was observed in the superior colliculus and the lateral geniculate nucleus contralateral to CS-injected eyes for 6 and 15 weeks. A significant decrease in phosphorylated neurofilament heavy chain (pNFH)- immunoreactivity, an increase in Iba-1(+), ED1(+) (microglial markers), and glial fibrillary acidic protein (GFAP, astrocytes) (+) area, and signs of demyelination were observed in the ON at 6 and 15 weeks of ocular hypertension. Microglial reactivity involvement was examined through a daily treatment with minocycline (30 mg/kg, i.p.) for 2 weeks, after 4 weeks of ocular hypertension. Minocycline prevented the increase in Iba-1(+), ED-1(+), and GFAP(+) area, the decrease in pNFH immunoreactivity and myelination, and the deficit in anterograde transport induced by 6 weeks of ocular hypertension. Thus, minocycline might prevent early axoglial alterations in the glaucomatous proximal ON.