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The Journal of Neuroscience, September 15, 1999, 19(18):7823-7833
Tetanic Stimulation Leads to Increased Accumulation of
Ca2+/Calmodulin-Dependent Protein Kinase II via Dendritic
Protein Synthesis in Hippocampal Neurons
Yannan
Ouyang1,
Alan
Rosenstein1,
Gabriel
Kreiman1,
Erin M.
Schuman1, 2, and
Mary B.
Kennedy1
1 Division of Biology and 2 Howard Hughes
Medical Institute, California Institute of Technology, Pasadena,
California 91125
mRNA for the -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 -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 -CaMKII can be measured 100-200 µm 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.
Key words:
long-term potentiation; protein phosphorylation; synapse; synaptic regulation; synaptic plasticity; immunocytochemistry; hippocampal slices
Copyright © 1999 Society for Neuroscience 0270-6474/99/19187823-11$05.00/0
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