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Related Experiment Videos

Cyclic-nucleotide-gated channels mediate synaptic feedback by nitric oxide

A Savchenko1, S Barnes, R H Kramer

  • 1Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Florida 33101, USA.

Nature
|December 31, 1997
PubMed
Summary

Cyclic-nucleotide-gated (CNG) channels in cone photoreceptors regulate neurotransmitter release. Nitric oxide (NO) activates these channels, mediating synaptic transmission and presynaptic effects.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Vision Science

Background:

  • Cyclic-nucleotide-gated (CNG) channels in photoreceptors are crucial for phototransduction and adaptation.
  • In cone photoreceptors, CNG channels may also play a role in synaptic function, regulating neurotransmitter release.
  • Nitric oxide (NO) is a retrograde transmitter that influences synaptic transmission by increasing cyclic GMP.

Purpose of the Study:

  • To investigate the presence and function of CNG channels in cone terminals.
  • To determine if CNG channels regulate neurotransmitter release in response to nitric oxide (NO).
  • To elucidate the role of CNG channels in mediating the presynaptic effects of NO in cone photoreceptors.

Main Methods:

  • Experiments on intact retina to observe NO modulation of cone-horizontal cell synapses.

Related Experiment Videos

  • Studies on isolated cones to directly assess CNG channel localization and activation.
  • Application of NO donors (S-nitrosocysteine) and cGMP analogs (pCPT-cGMP) to trigger transmitter release.
  • Use of guanylate cyclase inhibitors to block NO-induced effects.

    • Main Results:

    • Endogenous NO was found to modulate synapses between cones and horizontal cells in the retina.
    • CNG channels are localized in clusters within cone terminals and can be activated by NO donors.
    • Both NO donors and cGMP analogs induced neurotransmitter release from cone terminals.
    • NO-induced transmitter release was dependent on CNG channel activation and could be blocked by guanylate cyclase inhibitors.

    Conclusions:

    • CNG channels are present in cone terminals and regulate neurotransmitter release.
    • NO elicits neurotransmitter release from cone terminals by activating CNG channels.
    • These findings expand the known functions of CNG channels to include synaptic transmission regulation and mediation of NO's presynaptic effects.