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Accumulation of Neurocan, a Brain Chondroitin Sulfate Proteoglycan, in Association with the Retinal Vasculature in RCS Rats

¹From the Wallenberg Retina Center, Department of Ophthalmology, and the ²Department of Experimental Pathology, Lund University, Lund, Sweden.

PURPOSE. To examine whether and how the retinal distribution of the chondroitin sulfate proteoglycan neurocan is affected after photoreceptor cell loss and whether it correlates with the multiple secondary cellular changes that accompany the photoreceptor degeneration.

METHODS. Retinas from normal rats (Sprague-Dawley; postnatal days [P]0–P70), RCS rats with dystrophic retinas (P0–P300), RCS-rdy⁺ congenic rats with nondystrophic retinas (P0–202), and rhodopsin mutant rats, P23H (P0–P257) and S334ter (P0–P220), were processed for immunohistochemistry using a polyclonal antibody to rat neurocan.

RESULTS. The overall distribution of neurocan was similar in all retinas examined. Neurocan immunostaining was detected over the nerve fiber layer, the plexiform layers, the photoreceptor outer segments region, and the ciliary epithelium. With age, labeling throughout the plexiform layers decreased continuously. In RCS rats however, conspicuous labeling was also seen in association with retinal vessels, from P15 onward.

CONCLUSIONS. Accumulation of neurocan in association with the retinal vasculature does not correlate with photoreceptor cell loss, because it was not observed in the rhodopsin mutant rats. During the earliest stages of the disease, accumulation of debris in the subretinal space in RCS rats may be sufficient per se to initiate a cascade of metabolic changes that result in accumulation of neurocan. With time, the neurocan accumulated perivascularly may, by interaction with other matrix molecules, modulate at least some of the vascular alterations observed in this animal model.

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