Abstract
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and the BK channel are enriched at the presynaptic nerve terminal, where CaMKII associates with synaptic vesicles whereas the BK channel colocalizes with voltage-sensitive Ca(2+) channels in the plasma membrane. Mounting evidence suggests that these two proteins play important roles in controlling neurotransmitter release. Presynaptic BK channels primarily serve as a negative regulator of neurotransmitter release. In contrast, presynaptic CaMKII either enhances or inhibits neurotransmitter release and synaptic plasticity depending on experimental or physiological conditions and properties of specific synapses. The different functions of presynaptic CaMKII appear to be mediated by distinct downstream proteins, including the BK channel.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Calcium Channels, N-Type / genetics
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Calcium Channels, N-Type / metabolism
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Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics
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Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
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Humans
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Large-Conductance Calcium-Activated Potassium Channels / metabolism*
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Neuronal Plasticity / physiology
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Neurotransmitter Agents / metabolism
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Presynaptic Terminals / metabolism*
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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Protein Subunits / genetics
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Protein Subunits / metabolism
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Ryanodine Receptor Calcium Release Channel / metabolism
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SNARE Proteins / metabolism
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Synapsins / genetics
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Synapsins / metabolism
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Synaptic Transmission / physiology*
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Synaptotagmins / metabolism
Substances
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Calcium Channels, N-Type
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Large-Conductance Calcium-Activated Potassium Channels
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Neurotransmitter Agents
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Protein Isoforms
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Protein Subunits
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Ryanodine Receptor Calcium Release Channel
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SNARE Proteins
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Synapsins
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voltage-dependent calcium channel (P-Q type)
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Synaptotagmins
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Calcium-Calmodulin-Dependent Protein Kinase Type 2