作者: Yiqin Zhang , Uwe Rauch , Maria-Thereza R. Perez
DOI: 10.1167/IOVS.02-0450
关键词: Anatomy 、 Retinal 、 Nerve fiber layer 、 Biology 、 Immunostaining 、 Cell biology 、 Retina 、 Chondroitin sulfate 、 Chondroitin sulfate proteoglycan 、 Photoreceptor cell 、 Neurocan
摘要: PURPOSE. To examine whether and how the retinal distribution of chondroitin sulfate proteoglycan neurocan is affected after photoreceptor cell loss it correlates with multiple secondary cellular changes that accompany degeneration. METHODS. Retinas from normal rats (Sprague-Dawley; postnatal days [P]0-P70), RCS dystrophic retinas (P0-P300) RCS-rdy + congenic nondystrophic (P0-202), rhodopsin mutant rats, P23H (P0-P257) S334ter (P0-P220), were processed for immunohistochemistry using a polyclonal antibody to rat neurocan. RESULTS. The overall was similar in all examined. Neurocan immunostaining detected over nerve fiber layer, plexiform layers, outer segments region, ciliary epithelium. With age, labeling throughout layers decreased continuously. In however, conspicuous also seen association vessels, P15 onward. CONCLUSIONS. Accumulation vasculature does not correlate loss, because observed rats. During earliest stages disease, accumulation debris subretinal space may be sufficient per se initiate cascade metabolic result time, accumulated perivascularly may, by interaction other matrix molecules, modulate at least some vascular alterations this animal model.