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Regulation of Synaptic Transmission by Presynaptic CaMKII and BK Channels

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Abstract

Ca2+/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 Ca2+ 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.

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Acknowledgements

This work was supported by the National Science Foundation (0619427) and National Institute Health (GM083049). I thank my son Kaijie Jeffrey Wang for helping with the figures.

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Correspondence to Zhao-Wen Wang.

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Wang, ZW. Regulation of Synaptic Transmission by Presynaptic CaMKII and BK Channels. Mol Neurobiol 38, 153–166 (2008). https://doi.org/10.1007/s12035-008-8039-7

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