Tetanic stimulation leads to increased accumulation of Ca2+/calmodulin-dependent protein kinase II via dendritic protein synthesis in hippocampal neurons

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 th e Schaffer collateral pathway causes an increase in the concentration of al pha-CaMKII in the dendrites of postsynaptic neurons. The increase is blocke d by anisomycin and is detected by both quantitative immunoblot and semiqua ntitative immunocytochemistry. The increase in dendritic alpha-CaMKII can b e measured 100-200 mu m away from the neuronal cell bodies as early as 5 mi n after a tetanus. Transport mechanisms for macromolecules from neuronal ce ll bodies are not fast enough to account for this rapid increase in distal portions of the dendrites. Therefore, we conclude that dendritic protein sy nthesis must produce a portion of the newly accumulated CaMKII. The increas e in concentration of dendritic CaMKII after tetanus, together with the pre viously 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 t hat are controlled through phosphorylation by CaMKII.