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. 2018 Jun 11;146(2):145–159. doi: 10.1111/jnc.14449

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© 2018 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Three‐pool model of CaMKIIβ in dendritic spines. CaMKIIβ is classified into three distinct pools: CaMKIIβ associated with drebrin, CaMKIIβ associated with post‐synaptic density (PSD), and CaMKIIβ free from PSD and drebrin (probably associated with F‐actin). (a) In the resting state, CaMKIIβ associated with drebrin predominates in dendritic spines, and maintains the spine structure by cooperating with drebrin in the core of the spines. (b) CaMKIIβ does not accumulate in dendritic spines in drebrin‐knockdown neurons because of the lack of drebrin in dendrites. Interestingly, the relative increase in CaMKIIβ associated with PSD, caused by a decrease in drebrin‐associated CaMKIIβ following drebrin knockdown, means that the stable fraction is larger than the control, even though CaMKIIβ is not accumulated in dendritic spines. (c) Glutamate stimulation activates CaMKIIβ, resulting in dissociation of CaMKIIβ from drebrin in parallel with drebrin exodus and association of CaMKIIβ with PSD. CaMKIIβ associated with PSD consequently predominates in the activated state in the dendritic spine. Stability of CaMKIIβ in this pool contributes the increase in the stable fraction of CaMKIIβ in the activated state. (d) Glutamate stimulation in drebrin‐knockdown neurons increases second pool of CaMKIIβ more than glutamate stimulation in normal neurons.