Ambient light regulates sodium channel activity to dynamically control retinal signaling

J Neurosci. 2007 Apr 25;27(17):4756-64. doi: 10.1523/JNEUROSCI.0183-07.2007.

Abstract

The retinal network increases its sensitivity in low-light conditions to detect small visual inputs and decreases its sensitivity in bright-light conditions to prevent saturation. However, the cellular mechanisms that adjust visual signaling in the retinal network are not known. Here, we show that voltage-gated sodium channels in bipolar cells dynamically control retinal light sensitivity. In dim conditions, sodium channels amplified light-evoked synaptic responses mediated by cone pathways. Conversely, in bright conditions, sodium channels were inactivated by dopamine released from amacrine cells, and they did not amplify synaptic inputs, minimizing signal saturation. Our findings demonstrate that bipolar cell sodium channels mediate light adaptation by controlling retinal signaling gain.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Ocular / physiology*
  • Amacrine Cells / cytology
  • Amacrine Cells / metabolism
  • Animals
  • Cell Communication / physiology
  • Dopamine / metabolism
  • Dopamine Agonists / pharmacology
  • Dopamine Antagonists / pharmacology
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • Light*
  • Lighting
  • Organ Culture Techniques
  • Patch-Clamp Techniques
  • Photic Stimulation
  • Receptors, Dopamine D1 / physiology
  • Retinal Bipolar Cells / cytology
  • Retinal Bipolar Cells / physiology*
  • Signal Transduction / physiology*
  • Sodium Channels / physiology*

Substances

  • Dopamine Agonists
  • Dopamine Antagonists
  • Receptors, Dopamine D1
  • Sodium Channels
  • Dopamine