A gap junction network of Amacrine Cells controls Nitric Oxide release (Jacoby et al 2018)


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Accession:262452
"... The effects of the neuromodulator nitric oxide (NO) have been studied in many circuits, including in the vertebrate retina, where it regulates synaptic release, gap junction coupling, and blood vessel dilation, but little is known about the cells that release NO. We show that a single type of amacrine cell (AC) controls NO release in the inner retina, and we report its light responses, electrical properties, and calcium dynamics. We discover that this AC forms a dense gap junction network and that the strength of electrical coupling in the network is regulated by light through NO. A model of the network offers insights into the biophysical specializations leading to auto-regulation of NO release within the network."
Reference:
1 . Jacoby J, Nath A, Jessen ZF, Schwartz GW (2018) A Self-Regulating Gap Junction Network of Amacrine Cells Controls Nitric Oxide Release in the Retina. Neuron 100:1149-1162.e5 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Realistic Network;
Brain Region(s)/Organism:
Cell Type(s): Retina amacrine cell;
Channel(s):
Gap Junctions: Gap junctions;
Receptor(s):
Gene(s):
Transmitter(s): NO;
Simulation Environment: MATLAB (web link to model); NEURON (web link to model);
Model Concept(s):
Implementer(s): Jessen, Zachary F ; Schwartz, Gregory W [greg.schwartz at northwestern.edu];
Search NeuronDB for information about:  NO;
(located via links below)
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