Opposite effects of nitric oxide on rod and cone photoreceptors of rat retina in situ.

In the light-adapted vertebrate retina, nitric oxide (NO) modulates synaptic transmission between photoreceptors and second-order neurons. Although NO is believed to be a mediator of adaptation, its effect on photoreceptors in situ is not known yet. Therefore, we studied rod and cone activities in rat eyes in situ, using the electroretinogram (ERG). Rod and cone ERGs were functionally isolated by intravitreal 20mM glutamate, which suppressed the activity of all retinal cells except rods and cones for about 90min. The addition of NO-donor, SNAP, to the glutamate solution decreased the amplitude of the rod single-flash ERG by approximately 40%, compared to the amplitude of the rod ERG isolated by glutamate alone, but it increased the amplitude of the isolated, intense paired-flash cone ERG by approximately 40%. An excess of the NO-scavenger, CPTIO, had no significant effect on either rod or cone ERGs. A broad-spectrum NO-synthase inhibitor, L-NAME, increased the amplitude of the rod ERG by approximately 50%, but had no significant effect on the cone ERG. We suggest that NO directly modulates the light-evoked activity of rod and cone photoreceptors in situ, but in opposite ways.