Mechanisms of CaMKII action in long-term potentiation.
basic_science · Level V
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- Record sourced from PubMed, PMID 22334212.
- Also identified by DOI 10.1038/nrn3192 and PMC identifier 4050655.
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Abstract
Long-term potentiation (LTP) of synaptic strength occurs during learning and can last for long periods, making it a probable mechanism for memory storage. LTP induction results in calcium entry, which activates calcium/calmodulin-dependent protein kinase II (CaMKII). CaMKII subsequently translocates to the synapse, where it binds to NMDA-type glutamate receptors and produces potentiation by phosphorylating principal and auxiliary subunits of AMPA-type glutamate receptors. These processes are all localized to stimulated spines and account for the synapse-specificity of LTP. In the later stages of LTP, CaMKII has a structural role in enlarging and strengthening the synapse.
Medical subject headings
- Calcium-Calmodulin-Dependent Protein Kinase Type 2
- Hippocampus
- Long-Term Potentiation
- Synapses