<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p>s of DBA/2J mice develop severe optic nerve degeneration (). () The complete absence of NOS2 did not prevent glaucomatous neurodegeneration as many nerves had severe axonal damage. () genotype had no effect on the distribution of nerve damage. Numbers of nerves by age, genotype and disease state were: (given as total number analyzed, genotype, number of that genotype with mild, moderate, severe glaucoma) 3.5 months 6 6,0,0; 7 7,0,0;11 11,0,0; 10–12 months 53 23,3,27; 53 21,9,23; 56 17,3,36 (P value for all comparisons > 0.3). Average counts of RGC layer neurons from mice of each genotype with either severe glaucomatous damage or no detectable glaucomatous damage (total number of cells of the 8 fields counted per retina; see methods). genotype conferred no differential protective effect to RGCs in eyes with different degrees of axon loss. RGCs comprise 45–50% of cells in the RGC layer [71] and so almost all RGCs were lost in mice with severe axon loss independent of genotype. Percentage of surviving cells; , 54.4% ± 1.5; , 54.6% ± 1.5; , 58.0% ± 2.5; P values for all comparisons > 0.28. Number of retinal flat mounts counted, (given as genotype, mild, severe) 9, 7; 12, 8; 8, 13. Bar = 100 μm
