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

Endophilin A1 Promotes Actin Polymerization in Dendritic Spines Required for Synaptic Potentiation.
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Endophilin A1 促进突触增强所需的树突棘肌动蛋白聚合

DOI:
10.3389/fnmol.2018.00177
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发表时间:
2018
影响因子:
4.8
通讯作者:
Liu JJ
Liu JJ
中科院分区:
医学2区
文献类型:
--
作者:
Yang Y;Chen J;Guo Z;Deng S;Du X;Zhu S;Ye C;Shi YS;Liu JJ

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Endophilin A1是含有N-BAR结构域的endophilin A蛋白家族的成员,其参与膜动力学和运输。在突触前末梢,内嗜蛋白A参与突触囊泡的回收和自噬体的形成。通过基因敲除的研究,我们发现突触后的endophilin A1在突触可塑性中起作用。消融成熟小鼠海马CA 1区的内啡肽A1损害长期空间和背景恐惧记忆。其损失在CA 1神经元突触后的Schaffer侧支通路的损害,其AMPA型谷氨酸受体介导的突触传递和长时程增强。在KO神经元中,树突棘的结构和功能可塑性缺陷可以通过过度表达内啡肽A1而不是A2或A3来挽救。此外,在突触增强过程中,endophilin A1促进树突棘中的肌动蛋白聚合。这些发现揭示了不同的其他endophilin作为在突触后位点的endophilin A1的生理作用。
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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