Neuron
Volume 100, Issue 5, 5 December 2018, Pages 1149-1162.e5
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Article
A Self-Regulating Gap Junction Network of Amacrine Cells Controls Nitric Oxide Release in the Retina

https://doi.org/10.1016/j.neuron.2018.09.047Get rights and content
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Highlights

  • nNOS-2 amacrine cells are the main source of nitric oxide (NO) in the inner retina

  • These cells release NO rapidly upon light-induced depolarization

  • nNOS-2 amacrine cells are electrically coupled in the dark and decouple with NO

  • This network demonstrates a new auto-regulation mechanism for NO release

Summary

Neuromodulators regulate circuits throughout the nervous system, and revealing the cell types and stimulus conditions controlling their release is vital to understanding their function. 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.

Keywords

retina
nitric oxide
gap junctions
amacrine cell
NOS
nNOS
nNOS-2
Connexin-45
light adaptation

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