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Updated: Aug 29, 2026

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
Published on: July 17, 2011
Contribution of transient receptor potential channels to the control of GABA release from dendrites
Thomas Munsch1, Marc Freichel, Veit Flockerzi
1Institut für Physiologie, Medizinische Fakultät, Otto-von-Guericke Universität, Leipzigerstrasse 44, D-39120 Magdeburg, Germany.
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.
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