Frontiers in Molecular Neuroscience (May 2018)

Endophilin A1 Promotes Actin Polymerization in Dendritic Spines Required for Synaptic Potentiation

  • Yanrui Yang,
  • Yanrui Yang,
  • Jiang Chen,
  • Zhenzhen Guo,
  • Zhenzhen Guo,
  • Zhenzhen Guo,
  • Shikun Deng,
  • Shikun Deng,
  • Shikun Deng,
  • Xiangyang Du,
  • Xiangyang Du,
  • Shaoxia Zhu,
  • Shaoxia Zhu,
  • Chang Ye,
  • Yun S. Shi,
  • Jia-Jia Liu,
  • Jia-Jia Liu,
  • Jia-Jia Liu

DOI
https://doi.org/10.3389/fnmol.2018.00177
Journal volume & issue
Vol. 11

Abstract

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Endophilin A1 is a member of the N-BAR domain-containing endophilin A protein family that is involved in membrane dynamics and trafficking. At the presynaptic terminal, endophilin As participate in synaptic vesicle recycling and autophagosome formation. By gene knockout studies, here we report that postsynaptic endophilin A1 functions in synaptic plasticity. Ablation of endophilin A1 in the hippocampal CA1 region of mature mouse brain impairs long-term spatial and contextual fear memory. Its loss in CA1 neurons postsynaptic of the Schaffer collateral pathway causes impairment in their AMPA-type glutamate receptor-mediated synaptic transmission and long-term potentiation. In KO neurons, defects in the structural and functional plasticity of dendritic spines can be rescued by overexpression of endophilin A1 but not A2 or A3. Further, endophilin A1 promotes actin polymerization in dendritic spines during synaptic potentiation. These findings reveal a physiological role of endophilin A1 distinct from that of other endophilin As at the postsynaptic site.

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