ausblenden:
Schlagwörter:
Afferent Pathways/physiology
Animals
Anisomycin/pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases/*genetics
Corpus Striatum/*physiology
Dendrites/drug effects/*enzymology
Electric Stimulation
*Gene Expression Regulation, Enzymologic
Hippocampus/*physiology
In Vitro Techniques
Long-Term Potentiation/drug effects/*physiology
Male
Neurons/drug effects/enzymology/*physiology
Phosphorylation
Rats
Rats, Sprague-Dawley
Zusammenfassung:
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.
