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T.D. Kimble, M.E. C. Fitzgerald, A.J. Reiner; Photoreceptor Degeneration in Pigeons following Loss of Adaptive Parasympathetic Neural Control of Choroidal Blood Flow (ChBF) . Invest. Ophthalmol. Vis. Sci. 2004;45(13):40.
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Purpose: The medial part of the nucleus of Edinger–Westphal (EWM) in birds mediates light–regulated control of ChBF via the ciliary ganglion (Fitzgerald et al., 1996). Lesions of EWM reduce basal ChBF and prevent light–induced reflexive increases in ChBF (Fitzgerald et al., 1996). EWM–lesions have been shown to result in GFAP upregulation in Müller cells, indicative of retinal abnormality (Fitzgerald et al, 1990b). Behavioral studies of EWM lesioned birds have demonstrated significant acuity loss at a year post lesion (Hodos et al, 1998). In this study, we sought to determine if photoreceptor degeneration might account for acuity deficits in pigeons after an EWM lesion. Methods: Birds surviving up to 36 weeks after unilateral or bilateral electrolytic lesions of EWM were used. Eyes were processed for electron microscopy, and toluidine blue–stained semi–thin retinal sections were analyzed using light microscopy. For each case, sections in the high acuity area within the superior central retinal quadrant were analyzed. Characterization of photoreceptor degeneration included qualitative and quantitative assessments of the outer segment layer (OSL; disorganization, thinning, and abundance), inner segment layer (ISL; darkening, thinning, and vacuolization), and outer nuclear layer (ONL; darkened profiles, layer thickness, and cell body abundance). Results: In the retina of a 1–week old post–EWM lesioned bird, the OSL appeared normal with a regular array of OS and IS. By 16 weeks post–EWM lesion, there was a 45–50% reduction in OS abundance. There appeared to be many degenerated IS, some of which could be traced to darkened, shrunken or missing OS. There was no change in ONL thickness but there was an obvious decline in ONL cellular abundance, as well as many darkened cells with clumped nuclear chromatin. Many of the darkened cell bodies were continuous with darkened IS. Between 16 weeks and 36 weeks post–EWM lesion, there was a near complete loss of cone OS. The majority of IS were thin and exhibited vacuolization or lysis. ONL thickness was reduced to 84% of normal and the remaining cells appeared shrunken and many exhibited darkened cytoplasm with clumped nuclear material. Conclusions: These results show that loss of adaptive parasympathetic neural control of ChBF due to an EWM lesion causes progressive photoreceptor degeneration. The degeneration observed by 36 weeks post–EWM lesion might contribute to the decline in visual acuity noted in post–EWM lesioned birds (Hodos et al, 1998). Thus, impaired parasympathetic neural control of ChBF causes photoreceptor pathology.
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