Changes in the expression of the Y1 receptor of neuropeptide induced by photic injury

AV TORBIDONI, MP POSSIDENTE, MV CANTÓ-SOLER, T HÖKFELT, MJ VILLAR AND AM SUBURO

Buenos Aires, Argentina.

Congreso; Eighteenth Biennial Meeting of the International Society for Neurochemistry (ISN) and Thirty-Second Annual Meeting of the American Society for Neurochemistry (ASN); 2001

We have previously shown that in retinal detachment and proliferative vitreoretinopathy, the Y1 receptor of neuropeptide Y is up-regulated in Müller glial cells. Since the photoreceptor degeneration accompanying retinal light damage results in alterations of glial Müller cells, we compared immunoreactivity of glial fibrillary acidic protein (GFAP-ir) and Y1 (Y1-ir) in retina of BALB/c mice submitted to photic injury. These were housed under continuous illumination (3000lux) for 3-18days, whereas controls remained under normal circadian rhythm (˂300). Animals were perfused, and the eyes were cryosectioned, incubated with primary antibodies and developed using biotinylated peroxidase or double labeling with fluorescent secondary antibodies. Immunostaining of the inner retina was evaluated using an arbitrary density scale. Increases of GFAP-ir were detected at 3 days, but Y1-ir augmented only after 6days, when photoreceptor attrition began. Expression of both markers in the inner retina was maximal at 18days. Fluorescent double labelling demonstrated that in control animals Y1-ir was mainly restricted to ganglion cells. After photic injury, Y1-ir also appeared in Müller processes, particularly those around blood vessels. The express of Y1 mRNA was confirmed by RT-PCR. These findings confirm the presence of the Y1 receptor in injured Muller cells and suggest that this signalling pathway might play a role in trophic interactions between neurons and glia.