| First Author | Munsch T | Year | 2003 |
| Journal | Proc Natl Acad Sci U S A | Volume | 100 |
| Issue | 26 | Pages | 16065-70 |
| PubMed ID | 14668438 | Mgi Jnum | J:88211 |
| Mgi Id | MGI:3029676 | Doi | 10.1073/pnas.2535311100 |
| Citation | Munsch T, et al. (2003) Contribution of transient receptor potential channels to the control of GABA release from dendrites. Proc Natl Acad Sci U S A 100(26):16065-70 |
| abstractText | 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. |
