Translocation of CaMKII to dendritic microtubules supports the plasticity of local synapses |
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Authors: | Mado Lemieux Simon Labrecque Christian Tardif étienne Labrie-Dion éric LeBel Paul De Koninck |
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Institution: | 1Institut universitaire en santé mentale de Québec, Québec G1J 2G3, Canada;2Département de Biochimie, Microbiologie et Bio-informatique, Université Laval, Québec G1V 0A6, Canada |
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Abstract: | The processing of excitatory synaptic inputs involves compartmentalized dendritic Ca2+ oscillations. The downstream signaling evoked by these local Ca2+ transients and their impact on local synaptic development and remodeling are unknown. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an important decoder of Ca2+ signals and mediator of synaptic plasticity. In addition to its known accumulation at spines, we observed with live imaging the dynamic recruitment of CaMKII to dendritic subdomains adjacent to activated synapses in cultured hippocampal neurons. This localized and transient enrichment of CaMKII to dendritic sites coincided spatially and temporally with dendritic Ca2+ transients. We show that it involved an interaction with microtubular elements, required activation of the kinase, and led to localized dendritic CaMKII autophosphorylation. This process was accompanied by the adjacent remodeling of spines and synaptic AMPA receptor insertion. Replacement of endogenous CaMKII with a mutant that cannot translocate within dendrites lessened this activity-dependent synaptic plasticity. Thus, CaMKII could decode compartmental dendritic Ca2+ transients to support remodeling of local synapses. |
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