Nitric oxide modulates the transfer function between cones and horizontal cells during changing conditions of ambient illumination.
It has been suggested that nitric oxide (NO) serves as a retinal neuromodulator, adjusting retinal function to changing conditions of adaptation. We tested this hypothesis in the intact turtle retina by recording the photoresponses of L-cones and L1-horizontal cells, while changing retinal NO level and background illumination. Raising the retinal level of NO, by adding an NO donor (sodium nitroprusside) or the precursor for NO synthesis (L-arginine), induced response augmentation in L-cones and L1-horizontal cells. Lowering retinal level of NO by adding L-NAME, an inhibitor of NO synthesis, reduced the amplitudes of the photoresponses in these retinal neurons. The transfer function between L-cones and L1-horizontal cells, constructed from the photoresponses of these cells, was modified by NO and by background lights. The nonlinear transfer function, characteristic of the dark-adapted retina, became linear and of low gain when the retinal NO level was increased or by increasing the level of ambient illumination. In contrast, inhibiting NO synthesis in the light-adapted retina induced nonlinearity in the cone-to-horizontal cell transfer function similar to that seen in the dark-adapted state. NADPH diaphorase histochemistry, conducted on isolated retinal cells, demonstrated activity in cone inner segments and distal process of Müller cells. These findings support the hypothesis that NO synthesis in the distal turtle retina is triggered by background illumination, and that NO acts to adjust the modes of visual information processing in the outer plexiform layer to the conditions required during continuous background illumination.
Levy
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The Ruth & Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology and the Rappaport Institute, P.O.Box 9649, Haifa 31096, Israel.
Twig
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Perlman
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D000222:Adaptation, Physiological / Q000187:drug effects / Q000528:radiation effects; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D008029:Lighting; D008564:Membrane Potentials / Q000187:drug effects / Q000528:radiation effects; D009252:NADPH Dehydrogenase / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D012160:Retina / Q000166:cytology*; D017949:Retinal Cone Photoreceptor Cells / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D009435:Synaptic Transmission / Q000187:drug effects / Q000528:radiation effects; D014426:Turtles
D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D009599:Nitroprusside; D009569:Nitric Oxide; D001120:Arginine; D009252:NADPH Dehydrogenase; D019331:NG-Nitroarginine Methyl Ester; D004298:Dopamine