Shootin1a-Mediated Actin–Adhesion Coupling Generates Force to Trigger Structural Plasticity of Dendritic Spines

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 spines.

However, the molecular machinery that suffices for this 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.