Shootin1a-mediated actin-adhesion coupling generates force to trigger structural plasticity of dendritic spines

Cell Reports

Takeo Saneyoshi¹  Yasunori Hayashi¹  Kentarou Baba²  Hiroko Katsuno-Kambe²  Singh Saranpal²  Naoyuki Inagaki²  Ria Fajarwati Kastian²  Takunori Minegishi² 

[1] Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan;Laboratory of Systems Neurobiology and Medicine, Division of Biological Science, Nara Institute of Science and Technology, Ikoma, Nara 630-0192, Japan;

关键词: dendritic spine;    synaptic plasticity;    actin filaments;    shootin1;    N-cadherin;    L1-CAM;   

DOI  :  

来源: DOAJ

【 摘 要 】

Summary: Dendritic spines constitute the major compartments of excitatory post-synapses. They undergo activity-dependent enlargement, which is thought to increase the synaptic efficacy underlying learning and memory. The activity-dependent spine enlargement requires activation of signaling pathways leading to promotion of actin polymerization within the spines. However, the molecular machinery that suffices for that structural plasticity remains unclear. Here, we demonstrate that shootin1a links polymerizing actin filaments in spines with the cell-adhesion molecules N-cadherin and L1-CAM, thereby mechanically coupling the filaments to the extracellular environment. Synaptic activation enhances shootin1a-mediated actin-adhesion coupling in spines. Promotion of actin polymerization is insufficient for the plasticity; the enhanced actin-adhesion coupling is required for polymerizing actin filaments to push against the membrane for spine enlargement. By integrating cell signaling, cell adhesion, and force generation into the current model of actin-based machinery, we propose molecular machinery that is sufficient to trigger the activity-dependent spine structural plasticity.

【 授权许可】

Unknown