Contribution of transient receptor potential channels to the control of GABA release from dendrites.
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.
Munsch
Thomas
T
Institut für Physiologie, Medizinische Fakultät, Otto-von-Guericke Universität, Leipzigerstrasse 44, D-39120 Magdeburg, Germany.
Freichel
Marc
M
Flockerzi
Veit
V
Pape
Hans-Christian
HC
D000818:Animals; D015220:Calcium Channels / Q000502:physiology*; D003712:Dendrites / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D051381:Rats; D020318:Rats, Long-Evans; D018079:Receptors, GABA / Q000187:drug effects / Q000502:physiology*; D011985:Receptors, Serotonin / Q000502:physiology; D050052:TRPC Cation Channels; D013779:Tetrodotoxin / Q000494:pharmacology; D013788:Thalamus / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D015220:Calcium Channels; D018079:Receptors, GABA; D011985:Receptors, Serotonin; D050052:TRPC Cation Channels; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid