Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1149-1162.e5 |
| Journal | Neuron |
| Volume | 100 |
| Issue number | 5 |
| DOIs | |
| State | Published - Dec 5 2018 |
Funding
We thank our lab manager, Susan Wohlgenant, for her never-ending assistance with experimental preparation, antibody staining, and oversight of our mouse colonies and breeding. We also thank Steve DeVries and Yongling Zhu for providing the original mice used to make the preliminary findings on this project and for supplemental mice throughout the project and Petri Ala-Laurila, Fred Rieke, Mike Manookin, Will Grimes, Tiffany Schmidt, and Felice Dunn for their comments on early drafts of the manuscript. This research project was funded by Ruth L. Kirschstein National Research Service Award (NRSA) postdoctoral fellowship 1F32EY025930 -01, NIH DP2-DEY026770A and T32GM008152 , and the Research to Prevent Blindness Career Development Award.
Keywords
- Connexin-45
- NOS
- amacrine cell
- gap junctions
- light adaptation
- nNOS
- nNOS-2
- nitric oxide
- retina
ASJC Scopus subject areas
- General Neuroscience