| Annotated protein: | BDNF/NT-3 growth factors receptor (EC 2.7.10.1) (GP145-TrkB/GP95-TrkB) (Trk-B) (Neurotrophic tyrosine kinase receptor type 2) (TrkB tyrosine kinase). Gene symbol: NTRK2. Taxonomy: Mus musculus (Mouse). Uniprot ID: P15209 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ NTRK2 |
| Ontology domain: | Biological Process |
| SynGO term: | trans-synaptic signaling by BDNF, modulating synaptic transmission (GO:0099183) |
| Synapse type(s): | striatum |
| Annotated paper: | Plotkin JL, et al. "Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease" Neuron. 2014 Jul 2;83(1):178-88 PMID:24991961 |
| Figure(s): | Fig.3 |
| Annotation description: | Transsynaptic effects of TrkB are hard to find in literature. Many papers mention postsynatpic effects BDNF/trkb, but for transsynaptic signaling the source of BDNF and the location of Trkb are important. Very few papers show this apart from [pmid:24991961], a very complicated paper, but showing presynaptic release of BDNF onto striatal neurons that require TrkB for a response. 11/12/2017 Pim -This paper studies the BDNF communication between the presynaptic cortical neurons and postsynaptic spiny projection neurons (SPNs). The authors show that long-lasting enhancement in postsynaptic glutamate receptor currents that is known to be mediated by presynaptic release by cortical neurons of BDNF on these neurons (PMID:20980601), requires TrkB activation, postsynaptic NMDA receptors (NMDARs) and G-protein coupled receptors (GPCRs) linked to activation of protein kinase A (PKA) all in the postsynaptic compartment. - In my opinion the site of action for TrkB is not directly shown to be in the postsynapse, but I have allowed the term 'trans-synaptic' based on the authors intent: "Previous work had shown that corticostriatal long-term potentiation (LTP) in SPNs required BDNF activation of postsynaptic TrkBRs (Jia et al., 2010). This form of synaptic plasticity is postsynaptically induced and expressed, making it an ideal assay of postsynaptic TrkBR signaling." |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Electron Microscopy |
| Annotator(s): | Frank Koopmans (ORCID:0000-0002-4973-5732) Guus Smit (ORCID:0000-0002-2286-1587) Matthijs Verhage (ORCID:0000-0002-2514-0216) |
| Lab: | Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands |
| Additional literature: | PMID:24991961 states: "Previous work had shown that corticostriatal long-term potentiation (LTP) in SPNs required BDNF activation of postsynaptic TrkBRs (Jia et al., 2010). This form of synaptic plasticity is postsynaptically induced and expressed, making it an ideal assay of postsynaptic TrkBR signaling." @ PMID:20980601 |
| SynGO annotation ID: | 2108 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |