GIRARDI Elena Silvia
congresos y reuniones científicas
Effects of Adenosine A1 and A2a Receptors Modulation on Muller
MANUEL SOLINO, ESTER MARIA LOPEZ, LEONARDO JUAREZ, NOELI MARTIGNONE, ELENA GIRARDI, JUAN
Mar del Plata
Congreso; XXX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias (SAN),; 2015
Neurochemistry and NeuropharmacologyP210.-Effects of Adenosine A1 and A2a Receptors Modulation on MullerCell Activation in Light Induced Retinal DegenerationManuel Solino, Ester Maria Lopez, Leonardo Juarez, Noeli Martignone, Elena Girardi, JuanJose Lopez-CostaInstituto de Biologia Celular y Neurociencia ?dProf. E. De Robertis?d; Facultad de Me- dicina, UBACONICET,Buenos Aires, ARGENTINAsolino.firstname.lastname@example.org_____________________________________________________________Light induced retinal degeneration (LIRD) resembles retinal degenerative diseases and is auseful model to search for neuroprotective drugs. The modulation of adenosine A1 andA2a receptors have been proved to be neuroprotective in acute retinal injury, and indiverse CNS pathologies. The aim of this work was to evaluate the potentialneuroprotective effect of A1 and A2a agonists and antagonists on Muller 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 (A2aantagonist). Contralateral eyes were injected with respective vehicles as control. Then, ratswere submitted to continuous illumination (12000 lux) during 1 day. Retinas wereprocessed by GFAP immunocytochemistry. GFAP immunoreactive areas were quantifiedusing Fiji image analysis, and data were statistically analysed using Student?fs t test. Animalstreated with CPA showed a diminution in GFAP expression (P< 0.0001). The same trendwas seen after SCH 58261 treatment. On the opposite, eyes treated with DCPCX and withCGS 21680 showed a rise in GFAP (P<0.05 and P<0.001, respectively).Our results suggest that the activation of MCs is controlled by adenosine mediatedtransmission. As MCs have pro and antiapoptotic effects, we sustain that adenosinereceptor modulation is a plausible therapeutic strategy being A1 agonist and A2aantagonist drugs neuroprotective.(Supported by CONICET PIP1098 and UBACYT 20020100100329).