Wnt Signaling Mediates LTP-Dependent Spine Plasticity and AMPAR Localization through Frizzled-7 Receptors | Zendy

Faye McLeod | Zendy; Alessandro Bossio | Zendy; Aude Marzo | Zendy; Lorenza Ciani | Zendy; Sara Sibilla | Zendy; Saad Hannan | Zendy; Gemma A. Wilson | Zendy; Ernest Palomer | Zendy; Trevor G. Smart | Zendy; Alasdair J. Gibb | Zendy; Patricia C. Salinas | Zendy

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Wnt Signaling Mediates LTP-Dependent Spine Plasticity and AMPAR Localization through Frizzled-7 Receptors

Author(s) -

Faye McLeod,

Alessandro Bossio,

Aude Marzo,

Lorenza Ciani,

Sara Sibilla,

Saad Hannan,

Gemma A. Wilson,

Ernest Palomer,

Trevor G. Smart,

Alasdair J. Gibb,

Patricia C. Salinas

Publication year - 2018

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2018.03.119

Subject(s) - long term potentiation , ampa receptor , synaptic plasticity , dendritic spine , neuroscience , frizzled , excitatory postsynaptic potential , microbiology and biotechnology , long term depression , retrograde signaling , metaplasticity , biology , wnt signaling pathway , chemistry , glutamate receptor , signal transduction , receptor , hippocampal formation , biochemistry , inhibitory postsynaptic potential

The structural and functional plasticity of synapses is critical for learning and memory. Long-term potentiation (LTP) induction promotes spine growth and AMPAR accumulation at excitatory synapses, leading to increased synaptic strength. Glutamate initiates these processes, but the contribution from extracellular modulators is not fully established. Wnts are required for spine formation; however, their impact on activity-mediated spine plasticity and AMPAR localization is unknown. We found that LTP induction rapidly increased synaptic Wnt7a/b protein levels. Acute blockade of endogenous Wnts or loss of postsynaptic Frizzled-7 (Fz7) receptors impaired LTP-mediated synaptic strength, spine growth, and AMPAR localization at synapses. Live imaging of SEP-GluA1 and single-particle tracking revealed that Wnt7a rapidly promoted synaptic AMPAR recruitment and trapping. Wnt7a, through Fz7, induced CaMKII-dependent loss of SynGAP from spines and increased extrasynaptic AMPARs by PKA phosphorylation. We identify a critical role for Wnt-Fz7 signaling in LTP-mediated synaptic accumulation of AMPARs and spine plasticity.

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