New perspectives in glaucoma: unrecognized symptoms and looking for new therapeutic strategies.

ROSENSTEIN RE; DE ZAVALÍA, NURIA; KELLER SARMIENTO MI; LANZANI, MF; BELFORTE NA

Potrero de los Funes, San Luis

Simposio; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB), Simposio de Neurociencias; 2011

XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB)

Presentación Power Point Glaucoma is a leading cause of blindness, due to retinal ganglion cells (RGC) death and optic nerve damage. Retinal ischemia participates in glaucomatous damage. Recent evidences indicate that a population of RGC is intrinsically photosensitive (through the expression of a fotopigment, melanopsin), and transmits light information to the suprachiasmatic nuclei (SCN), the principal pacemaker for circadian rhythms. We analyzed: 1) the effect of ischemic conditioning on retinal damage induced by experimental glaucoma, and 2) the non-image forming visual system in experimental and human glaucoma. Weekly injections of vehicle or chondroitin sulfate were performed in the rat eye anterior chamber for 10 weeks. Ischemic conditioning was induced by weekly increasing intraocular pressure to 120 mmHg for 5 min. Brief ischemia pulses reversed the effect of glaucoma on retinal function and histology. Experimental glaucoma induced alterations in melanopsin levels, light suppression of nocturnal pineal melatonin, and light-induced c-Fos expression in the SCN. Glaucomatous animals exhibited an increase in the diurnal activity, and glaucomatous patients showed a significant decrease in the sleep quality.  Conclusion: The induction of ischemic tolerance could constitute a new therapeutic strategy for glaucoma treatment. Glaucoma induced significant alterations in the non-image forming visual system.