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

GONZÁLEZ FLEITAS MF; BORDONE MP; PASQUINI LA; BOSCO A; SANDE PH; DORFMAN D; ROSENSTEIN RE

Buenos Aires

Congreso; 2nd Congress of the Federation of Latin-American and Caribbean Societies for Neuroscience (FALAN); 2016

FALAN IBRO-LARC

S2P478. MINOCYCLINE PREVENTS EARLYAXOGLIAL ALTERATIONS OF THE OPTIC NERVEINDUCED BY EXPERIMENTAL GLAUCOMAMaría Flo rencia González Fleitas1,2,3,4*, MelinaPaula Bordone4,5,6,7, Laura A. Pasquini4,8,9, AlejandraBosco10, Pablo Sande1,2,3,4, Damián Dorfman1,2,3,4, RuthE. Rosenstein1,2,3,41 Laboratory of Retinal Neurochemistry and ExperimentalOphthalmology; 2 Department of Human Biochemistry; 3 Schoolof Medicine/CEFyBO; 4 University of Buenos Aires/CONICET ; 5Laboratory of Experimental Parkinson ; 6 ININFA; 7 FFyB; 8Department of Biological Chemistry and Institute of Chemistryand Biological Physicochemistry, IQUIFIB; 9 School of Pharmacyand Biochemistry; 10 Department of Neurobiology and Anatomy,University of Utah, Salt Lake City, Utah, USA*florgf88@gmail.comGlaucoma is a leading cause of blindness, characterizedby retinal ganglion cell (RGC) loss and optic nerve (ON)damage. Cumulative evidence suggests the participationof glial cells in the degeneration of the ON and RGCs.We analyze the effect of minocycline on early axoglialalterations of the ON in an experimental model of glaucomainduced by chondroitin sulfate (CS) injections into the eyeanterior chamber from Wistar rats. A significant decrease inBrn3a(+) RGC number was observed in eyes injected withCS at 10 weeks. A reduction in anterograde transport of Bsubunit cholera toxin (CTB) was observed in the superiorcolliculus and the lateral geniculate nucleus contralateral toCS-injected eyes for 6 and 15 weeks. A significant decreasein phosphorylated neurofilament heavy chain (pNFH)-immunoreactivity, an increase in Iba-1(+), ED1(+) (microglialmarkers), and glial fibrillary acidic protein (GFAP, astrocytes)(+) area, and signs of demyelination were observed in theON at 6 and 15 weeks of ocular hypertension. Microglialreactivity involvement was examined through a dailytreatment with minocycline (30 mg/kg, i.p.) for 2 weeks, after4 weeks of ocular hypertension. Minocycline preventedthe increase in Iba-1(+), ED-1(+), and GFAP(+) area, thedecrease in pNFH immunoreactivity and myelination, and the deficit in anterograde transport induced by 6 weeks ofocular hypertension. Thus, minocycline might prevent earlyaxoglial alterations in the glaucomatous proximal ON.