IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Müller cell activation in light induced retinal degeneration is prevented by adenosine receptors modulation
Autor/es:
SOLIÑO, M; LÓPEZ, EM; GIRARDI, E; BAREIRO, NM; LÓPEZ-COSTA, JJ
Lugar:
CABA
Reunión:
Congreso; Southamerican Neuroglia; 2017
Institución organizadora:
Polo Científico y Tecnológico
Resumen:
Müller cell gliosis is a component of retinal response to pathogenic stimuli which was observed in Light induced retinal degeneration (LIRD). Müller cells are important glial cells of the retina involved in ionic balance, glutamate uptake and synthesis of neurotrophic factors. LIRD resembles retinal degenerative diseases as AMD and is a useful model to search for neuroprotective drugs. The modulation of adenosine A1 and A2a receptors have been proved to be neuroprotective in acute retinal injury, and in diverse CNS pathologies. The aim of this work was to evaluate the potential neuroprotective effect of A1 and A2a agonists and antagonists on Müller cell (MC) activation using the model of LIRD.Sprague Dawley rats were intravitreally injected in one eye with one of the following drugs: CPA (A1 agonist); DCPCX (A1 antagonist); CGS 21680 (A2a agonist) or SCH 58261 (A2a antagonist). Contralateral eyes were injected with respective vehicles as control. Then, rats were submitted to continuous illumination (12000 lux) during 1 day. Retinas were processed by GFAP immunocytochemistry. GFAP immunoreactive areas were quantified using Fiji image analysis, and data were statistically analysed using Student´s t test. Animals treated with CPA showed a diminution in GFAP expression (P< 0.0001). The same trend was seen after SCH 58261 treatment. On the opposite, eyes treated with DCPCX and with CGS 21680 showed a rise in GFAP (P