The retinal spreading depression has been used as a tool to investigat
e the action of nitric oxide (NO) as a diffusible neurotransmitter whi
ch in many cases acts by raising the cGMP level in target cells. The r
ole of NO as a vasodilating agens has been well-established and it has
been suggested that the vasodilatation concurrent with cortical SD ma
y be mediated by NO. In this study, we present pure neuronal effects o
f NO on SD as the chicken retina is void of bloodvessels. We show that
NO directly decreases the velocity of retinal SD waves in a concentra
tion-and time-dependent manner. This effect can be partially mimicked
by application of membrane-permeable cGMP derivatives. Furthermore, a
NO-mediated speed up of the recovery of the intrinsic optical signal a
fter the wave-front is shown.