Activity-dependent synaptic Wnt release regulates hippocampal long term potentiation.
Wnts are important for various developmental and oncogenic processes. Here we show that Wnt signaling functions at synapses in hippocampal neurons. Tetanic stimulations induce N-methyl-d-aspartate receptor-dependent synaptic Wnt3a release, nuclear beta-catenin accumulations, and the activation of Wnt target genes. Suppression of Wnt signaling impairs long term potentiation. Conversely, activation of Wnt signaling facilitates long term potentiation. These findings suggest that Wnt signaling plays a critical role in regulating synaptic plasticity.
Chen
Jianyong
J
Department of Neurobiology and Behavior, Center for Neurobiology of Learning and Memory, University of California, Irvine, California 92697-3800, USA.
Park
Chang Sin
CS
Tang
Shao-Jun
SJ
D000200:Action Potentials; D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D017774:Long-Term Potentiation; D051379:Mice; D009474:Neurons / Q000378:metabolism; D015398:Signal Transduction; D009435:Synaptic Transmission; D051153:Wnt Proteins / Q000378:metabolism*; D060508:Wnt3 Protein; D060509:Wnt3A Protein; D051176:beta Catenin / Q000378:metabolism*
D051153:Wnt Proteins; D060508:Wnt3 Protein; D060509:Wnt3A Protein; C555511:Wnt3a protein, mouse; D051176:beta Catenin