Tetanic stimulation leads to increased accumulation of 
Ca(2+)/calmodulin-dependent protein kinase II via dendritic protein synthesis 
in hippocampal neurons

Ouyang, Y.; Rosenstein, A.; Kreiman, G.; Schuman, Erin M.; Kennedy, M. B.

doi:10.1523/JNEUROSCI.19-18-07823.1999

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Tetanic stimulation leads to increased accumulation of Ca(2+)/calmodulin-dependent protein kinase II via dendritic protein synthesis in hippocampal neurons

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Schuman, Erin M.
Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/10479685
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Citation

Ouyang, Y., Rosenstein, A., Kreiman, G., Schuman, E. M., & Kennedy, M. B. (1999). Tetanic stimulation leads to increased accumulation of Ca(2+)/calmodulin-dependent protein kinase II via dendritic protein synthesis in hippocampal neurons. J Neurosci, 19(18), 7823-33. doi:10.1523/JNEUROSCI.19-18-07823.1999.

Cite as: https://hdl.handle.net/21.11116/0000-0007-EF8E-D

Abstract

mRNA for the alpha-subunit of CaMKII is abundant in dendrites of neurons in the forebrain (Steward, 1997). Here we show that tetanic stimulation of the Schaffer collateral pathway causes an increase in the concentration of alpha-CaMKII in the dendrites of postsynaptic neurons. The increase is blocked by anisomycin and is detected by both quantitative immunoblot and semiquantitative immunocytochemistry. The increase in dendritic alpha-CaMKII can be measured 100-200 micrometer away from the neuronal cell bodies as early as 5 min after a tetanus. Transport mechanisms for macromolecules from neuronal cell bodies are not fast enough to account for this rapid increase in distal portions of the dendrites. Therefore, we conclude that dendritic protein synthesis must produce a portion of the newly accumulated CaMKII. The increase in concentration of dendritic CaMKII after tetanus, together with the previously demonstrated increase in autophosphorylated CaMKII (Ouyang et al., 1997), will produce a prolonged increase in steady-state kinase activity in the dendrites, potentially influencing mechanisms of synaptic plasticity that are controlled through phosphorylation by CaMKII.