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Synaptic plasticity

Pulling power of CAMK2α

Nature Reviews Neuroscience volume 11, page 223 (2010)Cite this article

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CAMK2α and CAMK2β are expressed in neurons, and their kinase activity contributes to synaptic plasticity. Upon neuronal activation, both isoforms move from the dendritic shaft to spines. The abundance of CAMK2 at synapses suggests that it may have an additional, structural role. Indeed, CAMK2β had been shown to mediate the reorganization of the actin cytoskeleton, but a structural role for CAMK2α had not been demonstrated.

In co-precipitation studies followed by mass spectrometry, the authors identified CAMK2α as a brain proteasome-associated protein. After demonstrating that CAMK2α and proteasomes colocalize in cultured rat hippocampal neurons, they showed in time lapse imaging studies that overexpression of CAMK2α enhanced NMDA (N-methyl-D-aspartate)-dependent recruitment of proteasomes to spines. By contrast, downregulation of CAMK2α expression by RNA interference or expression of mutant forms of CAMK2α that are deficient in activity-dependent translocation impaired this proteasome accumulation, suggesting a crucial role for CAMK2α in proteasome redistribution.

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References

ORIGINAL RESEARCH PAPER

  1. Bingol, B. et al. Autophosphorylated CaMKIIα acts as a scaffold to recruit proteasomes to dendritic spines. Cell 140, 567–578 (2010)

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FURTHER READING

  1. Tai, H.-C. & Schuman, E. M. Ubiquitin, the proteasome and protein degradation in neuronal function and dysfunction. Nature Rev. Neurosci. 9, 826–838 (2008)

    Article  CAS  Google Scholar 

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Authors
  1. Claudia Wiedemann
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Wiedemann, C. Pulling power of CAMK2α. Nat Rev Neurosci 11, 223 (2010). https://doi.org/10.1038/nrn2829

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