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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 gamma-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.

SUBMITTER: Munsch T

PROVIDER: S-EPMC307693 | biostudies-literature | 2003 Dec

REPOSITORIES: biostudies-literature

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Contribution of transient receptor potential channels to the control of GABA release from dendrites.

Munsch Thomas T Freichel Marc M Flockerzi Veit V Pape Hans-Christian HC

Proceedings of the National Academy of Sciences of the United States of America 20031210 26

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 gamma-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 ...[more]

PMID: 14668438

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