Reciprocal regulation of rod and cone synapse by NO (Kourennyi et al 2004)

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We constructed models of rod and cone photoreceptors using NEURON software to predict how changes in Ca channels would affect the light response in these cells and in postsynaptic horizontal cells.
1 . Kourennyi DE, Liu XD, Hart J, Mahmud F, Baldridge WH, Barnes S (2004) Reciprocal modulation of calcium dynamics at rod and cone photoreceptor synapses by nitric oxide. J Neurophysiol 92:477-83 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Retina photoreceptor cone cell;
Channel(s): I Chloride; I K; I h; I K,Ca; I Calcium; I Potassium;
Gap Junctions:
Transmitter(s): NO;
Simulation Environment: NEURON;
Model Concept(s): Calcium dynamics;
Implementer(s): Kourennyi, Dmitri E [dek at]; Liu, Xiaodong [xliu22 at];
Search NeuronDB for information about:  Retina photoreceptor cone cell; I Chloride; I K; I h; I K,Ca; I Calcium; I Potassium; NO;
This is the readme file for the model associated with the paper

Dmitri E. Kourennyi,1 Xiao-dong Liu,1 Jason Hart,4 Farid Mahmud,4
William H. Baldridge,2,3 and Steven Barnes3,5
Reciprocal Modulation of Calcium Dynamics at Rod and Cone
Photoreceptor Synapses by Nitric Oxide
J Neurophysiol 92: 477–483, 2004. First published February
25, 2004; 10.1152/jn.00606.2003. 

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

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 voltageindependent
conductance in both rods and cones. Suppression of NO
production in the intact retina with NG-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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The simulation will reproduce figure 4.

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