Molecules for memory: modelling CaMKII

Melanie Stefan, Nicolas Le Novère

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract / Description of output

Long-term modifications of synaptic strength, such as long-term potentiation (LTP) or long-term depression (LTD) are thought to underlie some forms of learning and memory. At the excitatory glutamate synapse, LTP is dependent on calcium influx through the N-methyl-D-aspartate (NMDA) receptor and subsequent activation of calcium/calmodulin-dependent protein kinase II (CaMKII). The NMDA receptor, CaMKII, and its activator calmodulin are all embedded in a complex hyperstructure consisting of more than 180 molecules [1] that acts as as a "synaptic plasticity nanomachine". Our current work aims at exploring CaMKII function in the context of the NMDA receptor complex
Original languageEnglish
Title of host publicationBMC Systems Biology
PagesP40
Volume1
EditionSuppl 1
DOIs
Publication statusPublished - 8 May 2007
Event BioSysBio 2007: Systems Biology, Bioinformatics, Synthetic Biology - Manchester, United Kingdom
Duration: 11 Jan 200713 Jan 2007

Publication series

NameBioSysBio 2007: Systems Biology, Bioinformatics, Synthetic Biology

Conference

Conference BioSysBio 2007: Systems Biology, Bioinformatics, Synthetic Biology
Country/TerritoryUnited Kingdom
CityManchester
Period11/01/0713/01/07

Keywords / Materials (for Non-textual outputs)

  • CaMKII
  • modelling
  • synapse

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