We investigated the expression of neuronal nitric oxide synthase (nNOS) in a rat retina model of chronic glaucoma, which was produced by electrocauterization of the episcleral vessels. Western-blot analysis showed that nNOS expression was significantly increased in cauterized retinas. nNOS immunoreactivity was observed in the cells of both the inner nuclear layer and the ganglion cell layer. Double labeling of retinal ganglion cells (RGCs) revealed that RGCs in the retina of cauterized rat was nNOS-immunopositive. Systemic administration of L-NAME (N(G)-nitro-L-arginine-methyl-ester), a non-specific NOS inhibitor, reduced RGC loss in cauterized rat retina, but there was no statistical significance (P =.06). These results suggest that the cytotoxicity of excessive NO plays a role in selective RGC loss in glaucoma.