The retinal spreading depression has been used as a tool to investigate the action of nitric oxide (NO) as a diffusible neurotransmitter which in many cases acts by raising the cGMP level in target cells. The role of NO as a vasodilating agens has been well-established and it has been suggested that the vasodilatation concurrent with cortical SD may be mediated by NO. In this study, we present pure neuronal effects of 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 concentration-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 after the wave-front is shown.
Brain Research – Elsevier
Published: Sep 11, 1995
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