ReviewNature reviews. Neuroscience2012
Mechanisms of CaMKII action in long-term potentiation.
Review in Nature reviews. Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 650 papers, 1 of them a synthesis that pooled it.
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Who cites it
650 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,113 citations in OpenAlex.
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- Molecular pathways for learning in the single-cell Stentor coeruleus.Current biology : CB · 2026Article
- Dynamic recruitment of CaMKII into SHANK3 phase-separated condensates tunes postsynaptic density remodeling during long-term potentiation.Nature communications · 2026Article
590 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.