CaMKII control of spine size and synaptic strength: Role of phosphorylation states and nonenzymatic action |
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| Authors: | Hyun Jae Pi Nikolai Otmakhov Farida El Gaamouch David Lemelin Paul De Koninck John Lisman |
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| Affiliation: | aQuantitative Biology Program, Physics Department, and;bVolen Center for Complex Systems, Biology Department, Brandeis University, Waltham, MA 02454; and;cCentre de Recherche, Université Laval Robert-Giffard, Quebec, QC, Canada, G1J 2G3 |
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| Abstract: | CaMKII is an abundant synaptic protein strongly implicated in plasticity. Overexpression of autonomous (T286D) CaMKII in CA1 hippocampal cells enhances synaptic strength if T305/T306 sites are not phosphorylated, but decreases synaptic strength if they are phosphorylated. It has generally been thought that spine size and synaptic strength covary; however, the ability of CaMKII and its various phosphorylation states to control spine size has not been previously examined. Using a unique method that allows the effects of overexpressed protein to be monitored over time, we found that all autonomous forms of CaMKII increase spine size. Thus, for instance, the T286D/T305D/T306D form increases spine size but decreases synaptic strength. Further evidence for such dissociation is provided by experiments with the T286D form that has been made catalytically dead. This form fails to enhance synaptic strength but increases spine size, presumably by a structural process. Thus very different mechanisms govern how CaMKII affects spine structure and synaptic function. |
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| Keywords: | synaptic plasticity structural plasticity autophosphorylation nonenzymatic function |
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