Abstract
Synaptic plasticity is thought to be a key process for learning, memory and other cognitive functions of the nervous system. The initial events of plasticity require the conversion of brief electrical signals into alterations of the biochemical properties of synapses that last for much longer than the initial stimuli. Here we show that a regulator of synaptic plasticity, calcium/calmodulin-dependent protein kinase IIalpha (CaMKII), sequentially translocates to postsynaptic sites, undergoes autophosphorylation and gets trapped for several minutes until its dissociation is induced by secondary autophosphorylation and phosphatase 1 action. Once dissociated, CaMKII shows facilitated translocation for several minutes. This suggests that trapping of CaMKII by its targets and priming of CaMKII translocation may function as biochemical memory mechanisms that change the signaling capacity of synapses.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aniline Compounds
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Animals
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Animals, Newborn
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases / drug effects
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cells, Cultured
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Electric Stimulation
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Fluorescent Dyes
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Glutamic Acid / metabolism
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Glutamic Acid / pharmacology
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Green Fluorescent Proteins
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / ultrastructure
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Indicators and Reagents / metabolism
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Luminescent Proteins / genetics
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Memory / physiology*
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Neuronal Plasticity / physiology*
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Neurons / drug effects
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Neurons / metabolism
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Neurons / ultrastructure
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Phosphorylation
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Synaptic Membranes / drug effects
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Synaptic Membranes / metabolism*
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Synaptic Membranes / ultrastructure
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Xanthenes
Substances
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Aniline Compounds
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Fluorescent Dyes
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Indicators and Reagents
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Luminescent Proteins
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Xanthenes
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Green Fluorescent Proteins
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Fluo-3
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Glutamic Acid
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases