IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
A1 receptor distribution in rat retina and its modifications after continuous illumination
Autor/es:
SOLIÑO M, LÓPEZ EM, GIRARDI E Y LÓPEZ-COSTA JJ
Lugar:
Huerta Grande-Córdoba
Reunión:
Congreso; XXVIII Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; 2013
Institución organizadora:
SAN
Resumen:
A1 RECEPTOR DISTRIBUTION IN RAT RETINA AND ITS MODIFICATIONS AFTER CONTINUOUS ILLUMINATION. Soliño M, López EM, Girardi E y López-Costa JJ. 1Instituto de Biología Celular y Neurociencia ¨Prof. E. De Robertis¨;  Facultad de Me- dicina, UBA-CONICET, Buenos Aires, ARGENTINA. Continuous illumination (CI) of rat retina produces photoreceptor degeneration. This model resembles human retinal degenerative diseases (AMD). Adenosine binds to four types of G protein coupled receptors named A1, A2A, A2B and A3. In the retina, A1 mRNA was reported in ganglion cell layer (GCL) by ISH. A1-agonists have shown a neuroprotective effect in acute retinal injury hence our interest in the study of this receptor. The aim was to map A1 in control (CTL) and illuminated (IL) rat retinas by immunocytochemistry. Sprague Dawley rats were submitted to CI (12000 lux) during 1, 2, 5 and 7 days. The eyes of CTL (n=2) and IL rats (n=8) were fixed by immersion in 4 % paraformaldehyde. Peroxidase inhibition was performed prior to immunostaining by PAP method using a rabbit polyclonal antibody to A1 (Santa Cruz Inc). CTL animals showed A1 immunoreactivity (A1-IR) in outer and inner plexiform layers and in ganglion cell layer (GCL). After 1 day of CI, A1-IR increased in GCL and in both plexiform layers. The increase of A1-IR persisted in GCL along the 7 days of CI, however A1-IR decreased in plexiform layers after 2 days of CI and increased again after 7 days of CI. Our results in CTL animals match the description accomplished by ISH and add A1-IR detection in plexiform layers. The peak of A1-IR at 24hs coexists with the previously determined maximum oxidative damage offering a suitable therapeutic target to  protect the retina from CI damage. (Supported by CONICET PIP1098 and UBACYT 20020100100329).