作者: Karam Kim , Gurpreet Lakhanpal , Hsiangmin E. Lu , Mustafa Khan , Akio Suzuki
DOI: 10.1016/J.NEURON.2015.07.023
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摘要: The structural modification of dendritic spines plays a critical role in synaptic plasticity. CaMKII is pivotal molecule involved this process through both kinase-dependent and independent functions, but the respective contributions these two functions to plasticity remain unclear. We demonstrate that transient interplay between kinase during induction temporally gates activity-dependent actin cytoskeleton. Inactive binds F-actin, thereby limiting access actin-regulating proteins F-actin stabilizing spine structure. CaMKII-activating stimuli trigger dissociation from specific autophosphorylation reactions within binding region permits remodeling by regulatory followed reassociation restabilization. Blocking impairs functional without affecting activity. These results underpin importance defining time window permissive for