Abstract
Purpose: :
The effects of aging on the visual system include a variety of degenerative and regressive events. In the retina loss of photoreceptors and ganglion cells has been documented in several species, including humans, but relatively little is known about age–related changes in other retinal cell types. In the present study we examine normal aging retina in C57/B6 mice and document an unexpected sprouting of rod bipolar cell dendrites into the outer plexiform layer (OPL).
Methods: :
Immunohistochemical and fluorescent imaging techniques were used to investigate rod bipolar cell dendritic morphology in young (3 to 6 months of age) and aged (> 1 year) mice. These cells were labeled with a PKC antibody and aberrant dendritic processes extending into the OPL were traced for quantitative analysis. Presynaptic sites were labeled with PSD–95 and the number of photoreceptors was determined by counting DAPI labeled profiles in the outer nuclear layer (ONL).
Results: :
Retinas of old mice had many rod bipolar cell dendrites that extended into the ONL. By contrast, these processes were strictly confined to the OPL in young adult mice. The number and length of the aberrant dendrites were found to increase with age, and their presence was evident at all retinal eccentricities. Furthermore, such processes were closely juxtaposed with the presynaptic sites of photoreceptors (labeled with PSD–95) suggesting that they form functional synapses. Detailed counts of photoreceptors in retinal sections of old animals containing the aberrant rod bipolar cell dendrites demonstrated no significant decline in the number of photoreceptors, a finding consistent with previously published findings in this mouse strain.
Conclusions: :
Our findings suggest that afferent cell loss is not the impetus for the age–related dendritic sprouting we observed. These results could be interpreted as reflecting a compensatory change in retinal neural circuitry during normal aging. This contrasts with the degenerative changes that have been noted previously at all other levels of the nervous system.
Keywords: aging • bipolar cells • plasticity