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This article is part of the supplement: Seventeenth Annual Computational Neuroscience Meeting: CNS*2008

Open Access Open Badges Lecture presentation

CaM kinases and AMPA receptor subunit recomposition in hippocampal synaptic plasticity

Victor Derkach

Author affiliations

Vollum Institute, Oregon Health and Science University, Portland, OR 97201-3098, USA

Citation and License

BMC Neuroscience 2008, 9(Suppl 1):L5  doi:10.1186/1471-2202-9-S1-L5

The electronic version of this article is the complete one and can be found online at:

Published:11 July 2008

© 2008 Derkach; licensee BioMed Central Ltd.

Lecture presentation

It is broadly believed that synaptic plasticity is a neuronal mechanism for learning and memory in the mammalian brain. In the mature hippocampus, the expression of long-term potentiation (LTP) in Schaffer collateral-CA1 synapses requires a postsynaptic Ca2+ influx and the GluR1 subunit of the AMPA subtype of glutamate receptor (AMPAR). New findings indicate that the pattern of synaptic activity associated with exploratory behavior can induce LTP by changing the quality of synaptic AMPARs. This process is dynamic and requires activity of Ca2+/calmodulin dependent protein kinases (CaMKs), key transducers of postsynaptic Ca2+ changes into LTP. The two CaMKs, CaMKI and CaMKII target AMPARs and regulate synaptic strength differently, however. Under basal conditions, AMPARs in these synapses are heteromers composed of GluR1 and GluR2 subunits. CaMKI enhances synaptic strength by trafficking to synapses more functionally efficient and highly Ca2+-permeable GluR2-lacking AMPARs through a regulated actin dynamics. In contrast, CaMKII can enhance functional properties of these GluR2-lacking AMPARs by a direct phosphorylation of the C-terminus of GluR1 subunit. Taken together, these results argue for two distinct but orchestrated mechanisms in modification of synaptic strength during LTP. Results are discussed in terms of the role of AMPAR subunit recomposition for synaptic plasticity.