期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：26
页码：16065-16070
DOI：10.1073/pnas.2535311100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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.
