Yannan Ouyang, Alan Rosenstein, Gabriel Kreiman, Erin M. Schuman and Mary B. Kennedy

Tetanic Stimulation Leads to Increased Accumulation of Ca2+ / Calmodulin-Dependent Protein Kinase II via Dendritic Protein Synthesis in Hippocampal Neurons

Journal of Neuroscience (1999) 19:7823–7833 PDF

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mRNA for the a-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 a-CaMKII in the dendrites of postsynaptic neurons. The increase is blocked by anisomycin and is detected by both quantitative immunoblot and semi-quantitative immunocytochemistry. The increase in dendritic a-CaMKII can be measured 100–200 mm 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 accu-mulated CaMKII. The increase in concentration of dendritic CaMKII after tetanus, together with the previously demon-strated 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.