In the mammalian retina, neuronal nitric oxide
synthase (NOS) is mainly localized in subpopulations of
amacrine cells. One function of nitric oxide (NO) is to
stimulate soluble guanylate cyclases which in turn synthesize
cGMP. We used an antibody specific for cGMP to demonstrate
cGMP-like immunoreactivity (cG-IR) in bovine, rat, and
rabbit retinae and investigated the effects on cGMP levels
of both exogenously applied NO and of endogenously released
NO. We found that cGMP levels in inner and outer retina
were controlled in opposite ways. In the presence of the
NO-donors SNP, SIN-1 or SNAP, cG-IR was prominent in neurons
of the inner retina, mainly in cone bipolar cells, some
amacrine and ganglion cells. Retinae incubated in IBMX
showed weak cG-IR in bipolar cells. Glutamate increased
cG-IR in the inner retina, presumably by stimulating endogenous
NO release, whereas NOS inhibitors or GABA and glycine
decreased cG-IR in bipolar cells by reducing NO release.
In somata, inner segments and spherules of rod photoreceptors
the situation was reversed. cG-IR was undetectable in the
presence of NO-donors or glutamate, was moderate in IBMX-treated
retinae, but increased strongly in the presence of NOS
inhibitors or GABA/glycine. We conclude that NO is released
endogenously in the retina. In the presence of NO, cGMP
levels are increased in neurons of the inner retina, but
are decreased in rods.