Mechanisms of CaMKII action in long-term potentiation

By John E. Lisman, R. Yasuda, Sridhar Raghavachari. Nature Reviews Neuroscience, 2012

1,104 citations recorded by the source corpus.

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.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d02618605d0a81024319aaecda0e260ff398d8c1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Y. Dudai
2. E. Kandel
3. T. Takeuchi
4. A. Duszkiewicz
5. M. Mayford
6. Richard G. M. Morris
7. C. Duarte
8. Graciano Leal

In Molecular Biology

1. C. Duarte
2. Graciano Leal
3. Diogo Comprido
4. Y. Dudai
5. Igor Timofeev
6. Richard G. M. Morris
7. Sylvain Chauvette
8. M. Mayford

Citations in the corpus

• BDNF-induced local protein synthesis and synaptic plasticity. (2014, positive): “The Ca2þ- and calmodulindependent protein kinase II is a major constituent of the PSD and plays a structural role in enlarging and strengthening the synapse in the late phases of LTP (Lisman et al., 2012).”
• Sleep oscillations in the thalamocortical system induce long-term neuronal plasticity (2012, positive): “Also, the translocation of AMPA receptors to the synapse (Lisman et al., 2012; Malinow and Malenka, 2002) that probably occurs during SWS does not require new gene expression.”
• The restless engram: consolidations never end. (2012, background): “This Ca signal can activate awide range of signaling pathways including CaMKII, PKC, PKA, and MAPK that have each been implicated in the induction of LTP as well as in its later stabilization (Malenka and Bear, 2004; Huang et al., 2013; Kerchner and Nicoll, 2008; Kessels and Malinow, 2009; Lisman et”
• The molecular and systems biology of memory. (2014, positive): “This Ca signal can activate awide range of signaling pathways including CaMKII, PKC, PKA, and MAPK that have each been implicated in the induction of LTP as well as in its later stabilization (Malenka and Bear, 2004; Huang et al., 2013; Kerchner and Nicoll, 2008; Kessels and Malinow, 2009; Lisman et”
• Spike-Timing Dependence of Structural Plasticity Explains Cooperative Synapse Formation in the Neocortex (2012, background): “A biochemical mechanism underlying this assumption could be the activation of a signaling pathway when a specific number of activated CaMKII molecules is reached [39].”
• The synaptic plasticity and memory hypothesis: encoding, storage and persistence (2014, background): “The now extensive list of mutated genes includes those coding for PSD scaffolding proteins [83], kinases and phosphatases [84–86], motor proteins [87,88], regulators for epigenetic mechanisms [89], translational regulators [9,90] and immediate early genes [91].”