4.8 Article

A Self-Regulating Gap Junction Network of Amacrine Cells Controls Nitric Oxide Release in the Retina

期刊

NEURON
卷 100, 期 5, 页码 1149-+

出版社

CELL PRESS
DOI: 10.1016/j.neuron.2018.09.047

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资金

  1. Ruth L. Kirschstein National Research Service Award (NRSA) [1F32EY025930-01]
  2. NIH [DP2-DEY026770A, T32GM008152]
  3. Research to Prevent Blindness Career Development Award
  4. NATIONAL EYE INSTITUTE [F32EY025930, DP2EY026770] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM008152] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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 neuro-modulator 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 autoregulation of NO release within the network.

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