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Reciprocal Modulation of Calcium Dynamics at Rod and Cone Photoreceptor Synapses by Nitric Oxide

¹Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106; Departments of ²Anatomy and Neurobiology, ³Ophthalmology and Visual Science, and ⁵Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia B3H 4H7; and ⁴Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta T2N 4N1, Canada

Submitted 25 June 2003; accepted in final form 16 February 2004

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.

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