Reciprocal modulation of calcium dynamics at rod and cone photoreceptor synapses by nitric oxide

J Neurophysiol. 2004 Jul;92(1):477-83. doi: 10.1152/jn.00606.2003. Epub 2004 Feb 25.


The abundance of nitric oxide (NO) synthesizing enzymes identified in the vertebrate retina highlight the importance of NO as a signaling molecule in this tissue. Here we describe opposing actions of NO on the rod and cone photoreceptor synapse. Depolarization-induced increases of calcium concentration in rods and cones were enhanced and inhibited, respectively, by the NO donor S-nitrosocysteine. NO suppressed calcium current in cones by decreasing the maximum conductance, whereas NO facilitated rod Ca channel activation. NO also activated a nonselective voltage-independent conductance in both rods and cones. Suppression of NO production in the intact retina with N(G)-nitro-l-arginine favored cone over rod driven postsynaptic signals, as would be expected if NO enhanced rod and suppressed cone synaptic activity. These findings may imply involvement of NO in regulating the strength of rod and cone pathways in the retina during different states of adaptation.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ambystoma
  • Animals
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology*
  • Enzyme Inhibitors / pharmacology
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / physiology*
  • Nitric Oxide Donors / pharmacology
  • Retinal Cone Photoreceptor Cells / drug effects
  • Retinal Cone Photoreceptor Cells / physiology*
  • Retinal Rod Photoreceptor Cells / drug effects
  • Retinal Rod Photoreceptor Cells / physiology*
  • Synapses / drug effects
  • Synapses / physiology*


  • Enzyme Inhibitors
  • Nitric Oxide Donors
  • Nitric Oxide