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Mechanism of TrkB-Mediated Hippocampal Long-Term Potentiation

descriptionPublicationkeyboard_double_arrow_right Article 01 Sep 2002 Italy English Publisher:Elsevier BVJournal:Neuron, volume 36, pages 121-137 (issn: 0896-6273,

Authors: Minichiello Liliana; Calella Anna Maria; Medina D; Bonhoeffer Tobias; Klein Rüdiger; Korte Martin;

doi: 10.1016/s0896-6273(02)00942-x

pmid: 12367511

handle: 11588/752953

Mechanism of TrkB-Mediated Hippocampal Long-Term Potentiation

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Abstract

The TrkB receptor tyrosine kinase and its ligand, BDNF, have an essential role in certain forms of synaptic plasticity. However, the downstream pathways required to mediate these functions are unknown. We have studied mice with a targeted mutation in either the Shc or the phospholipase Cgamma (PLCgamma) docking sites of TrkB (trkB(SHC/SHC) and trkB(PLC/PLC) mice). We found that hippocampal long-term potentiation was impaired in trkB(PLC/PLC) mice, but not trkB(SHC/SHC) mice. BDNF stimulation of primary neurons derived from trkB(PLC/PLC) mice fully retained their ability to activate MAP kinases, whereas induction of CREB and CaMKIV phosphorylation was strongly impaired. The opposite effect was observed in trkB(SHC/SHC) neurons, suggesting that MAPKs and CREB act in parallel pathways. Our results provide genetic evidence that TrkB mediates hippocampal plasticity via recruitment of PLCgamma, and by subsequent phosphorylation of CaMKIV and CREB.

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Italy

Related Organizations

University Federico II of Naples
Italy
Max Planck Society
Germany
European Molecular Biology Laboratory
Italy
National Institute for Nuclear Physics
Italy
European Molecular Biology Laboratory
Germany

Keywords

Binding Sites, General Neuroscience, Neuroscience(all), Brain-Derived Neurotrophic Factor, Long-Term Potentiation, Active Transport, Cell Nucleus, Mice, Transgenic, Hippocampus, Immediate-Early Proteins, DNA-Binding Proteins, Isoenzymes, Adaptor Proteins, Vesicular Transport, Mice, Fetus, Calcium-Calmodulin-Dependent Protein Kinases, Animals, Mitogen-Activated Protein Kinases, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Cyclic AMP Response Element-Binding Protein, Calcium-Calmodulin-Dependent Protein Kinase Type 4, Adaptor Proteins, Signal Transducing, Early Growth Response Protein 1

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