title: Changes in choroidal innervation in Royal College of Surgeons rats with hereditary retinal degeneration.
abstract: In Royal College of Surgeons (RCS) rats with hereditary retinal degeneration loss of retinal pigmented epithelium (RPE) and choriocapillaris is most pronounced in the upper-temporal quadrant. To investigate whether changes in choroidal vasodilative innervation might be involved in the RPE degeneration, we analyzed whole mount preparations of the retina and choroid stained for nitric oxide synthase and for NADPH-diaphorase (d) of 19 dystrophic RCS rats and 24 age-matched congenic controls of different age groups. Density of NADPH-d-positive nerve fibers was quantitatively evaluated in the upper-temporal and lower-nasal quadrant. Our results revealed that even in control animals there were much less positively stained nerve fibers in the upper-temporal than in the lower-nasal quadrant. Nerve fiber density in both quadrants increased for up to 3 months and remained nearly constant throughout life. In the dystrophic animals up to 3 months of age nerve fiber density was similar to that seen in the controls. In dystrophic animals older than 3 months nerve fiber density in the upper-temporal quadrant decreased significantly, whereas density in the lower-nasal quadrant revealed nearly the same values as in the age-matched controls. Decrease of NADPH-d stained nerve fibers in this quadrant occurred prior to the vascular changes in the choriocapillaris. In the retina of RCS dystrophic rats an increase of NADPH-d-positive amacrine cells was found only in 3-month-old animals. Most of these cells were located in the vicinity of irregularly arranged branches of the central retinal artery. In animals 5 months of age and older the number of cells decreased to the same values found in controls, so that we assume that increase of NADPH-d-positive amacrine cells is involved in capillary degeneration or sprouting.
authors.affiliation: Institute of Anatomy II, Friedrich Alexander University Erlangen-N urnberg, Erlangen, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Rexer
authors.forename: C A
authors.initials: CA
authors.lastname: May
authors.forename: E
authors.initials: E
authors.lastname: Lütjen-Drecoll
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000294:innervation; D002452:Cell Count; D002829:Choroid / Q000098:blood supply / Q000294:innervation* / Q000473:pathology; D007124:Immunoenzyme Techniques; D009252:NADPH Dehydrogenase / Q000378:metabolism; D009412:Nerve Fibers; D009474:Neurons / Q000201:enzymology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D051381:Rats; D011922:Rats, Mutant Strains; D012162:Retinal Degeneration / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D013564:Sympathetic Nervous System / Q000378:metabolism* / Q000473:pathology
chemical_list: D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D009252:NADPH Dehydrogenase