Abstract
Purpose: :
Participation of retinal ganglion produced melanopsin in circadian photoentrainment might be independent of classical rods and cones. However, no evidence shows that melanopsin–positive ganglion cells will always escape the influences of photoreceptors in other biological or pathological processes. In this study, we investigate the melanopsin production in retinal ganglion cells in a murine model of photoreceptor degeneration.
Methods: :
Photoreceptor degeneration in an animal model was induced by a single intraperitoneal injection of N–methyl–N–nitrosourea (MNU) in adult SD rats. 0.5, 1, 5, 7, 13 and 28 d after drug administration, expression of melanopsin was examined by fluorescent immunolabelling of fixed retina, and real–time quantitative RT–PCR for mRNA from the retina was performed.
Results: :
On d0.5, photoreceptors showed some signs of early apoptosis; on d7, the majority of photoreceptors had degenerated. Melanopsin mRNA decreased gradually associated with photoreceptor loss. At the same time, pituitary adenylate cyclase–activating polypeptide (PACAP), a protein colocalized with melanopsin in ganglion cells, did not exhibit much variability. During the process of photoreceptor degeneration, expression of melanopsin on ganglion dendrites faded away, while in the soma the expression persisted for a long time.
Conclusions: :
Our data suggest normal photoreceptors may be essential for the expression of melanopsin, at least in ganglion cell dendrites. This also means that melanopsin from different cellular locations may affect circadian systems in different ways. Because light stimuli also regulates production of melanopsin, photoreceptors might participate in circadian photoentrainment as well.
Keywords: photoreceptors • degenerations/dystrophies • ganglion cells