Acetylcholine is one of the primary excitatory
neurotransmitters/neuromodulators in the retina, but little is
known about the downstream signaling pathways it can activate. The
present study immunocytochemically examines the potential sources of
acetylcholine and the location of the nicotinic cholinergic receptors
in the turtle retina. It also examines how activation of these
receptors can influence the nitric oxide (NO)/cyclic guanosine
monophosphate (cGMP) signal-transduction pathways. Photoreceptors,
amacrine cells, and potentially ganglion cells contain choline
acetyltransferase-like immunoreactivity (LI). Nicotinic acetylcholine
receptors are immunocytochemically localized on photoreceptors,
horizontal, bipolar, and ganglion cells. Nitric oxide imaging indicates
that stimulation with nicotine increases NO production primarily in
photoreceptors, horizontal, Müller, bipolar, and ganglion cells.
In turn, very select populations of amacrine cells respond to this NO
with increased levels of cGMP-LI. Selective inhibitors reveal that
nitric oxide synthase is involved in most, but not all, of these
increases in cGMP-LI. These results show that acetylcholine can
activate the NO/cGMP signal-transduction pathways in both the inner
and outer retina. This indicates that both of the major excitatory
retinal transmitters, glutamate and acetylcholine, can stimulate NO
production that increases levels of cGMP-LI in overlapping populations
of retinal cells.