Nitric oxide (NO) activates soluble guanylyl cyclase (sGC)
and the resulting increase in cyclic guanosine monophosphate
(cGMP) is an important intracellular signalling pathway in the
vertebrate retina. Immunocytochemical detection of cGMP following
exposure to NO donors has proven an effective method of identifying
cells that express sGC. While such an approach has proven useful
for the study of several vertebrate retinas, it has not been
applied to the well-characterized teleost retina. Therefore,
in the present study, we have applied this approach to the retina
of the goldfish (Carassius auratus). In the presence of the
phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX),
incubation of goldfish eyecups in Ringer's solution containing
(±)-S-nitroso-N-acetylpenicillamine (SNAP) increased
cGMP-like immunoreactivity (cG-ir) in bipolar, horizontal,
amacrine, and ganglion cells and in ganglion cell axons and
optic nerve. Weak labeling was observed in horizontal cells
but no change in cG-ir was noted within photoreceptors. The
NO donor-stimulated increases of cG-ir in horizontal, bipolar,
amacrine, and ganglion cells are consistent with known
physiological effects of NO on these neurons. The physiological
significance of NO action at the level of optic nerve is not
known. The lack of an effect of SNAP on cG-ir in photoreceptors
was unexpected, as there are known physiological actions of
NO, mediated by cGMP, on these neurons. Although this may be
due to insufficient sensitivity of immunolabeling, this result
may indicate a difference between isoforms of sGC or cGMP PDE
in these neurons, compared to neurons where exogenous NO increased
cG-ir.
