Contribution of transient receptor potential channels to the control of GABA release from dendrites
Abstract
Neuronal dendrites have been shown to actively contribute to synaptic information transfer through the Ca2+-dependent release of neurotransmitter, although the underlying mechanisms remain elusive. This study shows that the increase in dendritic γ-aminobutyric acid (GABA) release from thalamic interneurons mediated by the activation of 5-hydroxytryptamine type 2 receptors requires Ca2+ entry that does not involve Ca2+ release nor voltage-gated Ca2+ channels in the plasma membrane but that is critically dependent on the transient receptor potential (TRP) protein TRPC4. These data ascribe a functional role of agonist-activated TRP channels to the release of transmitters from dendrites, thereby indicating a principle underlying synaptic interactions in the brain.
- Publication:
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Proceedings of the National Academy of Science
- Pub Date:
- December 2003
- DOI:
- 10.1073/pnas.2535311100
- Bibcode:
- 2003PNAS..10016065M
- Keywords:
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- Neuroscience