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Related Concept Videos

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Synaptic memory and CaMKII.

Roger A Nicoll1, Howard Schulman2,3

  • 1Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, California, United States.

Physiological Reviews
|June 8, 2023
PubMed
Summary
This summary is machine-generated.

Calcium/calmodulin-dependent protein kinase II (CaMKII) is crucial for synaptic plasticity and memory. This review details CaMKII

Keywords:
AMPA receptorCaMKIINMDA receptorcalciumlong-term potentiation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • CaMKII and LTP were discovered near-simultaneously and are closely linked.
  • CaMKII's proposed role as a memory molecule predates its physiological connection to LTP.
  • Decades of research and technological advancements have solidified CaMKII's role in synaptic physiology.

Purpose of the Study:

  • To review the historical linkage between CaMKII and LTP.
  • To present a model for synaptic memory involving CaMKII.
  • To critically assess the evidence supporting each step of the proposed model.

Main Methods:

  • In vitro brain slices
  • Mouse genetics
  • Single-cell molecular genetics
  • Pharmacological reagents
  • Protein structure analysis
  • Two-photon microscopy

Main Results:

  • CaMKII activation by NMDA receptor-mediated Ca2+ influx.
  • CaMKII autophosphorylation leads to sustained activity and GluN2B binding.
  • CaMKII-GluN2B complex formation induces postsynaptic density (PSD) structural rearrangement.
  • PSD remodeling involves PSD-95, AMPARs, and TARPs, increasing AMPARs and potentiating synapses.
  • CaMKII maintains potentiation through subunit exchange or phosphorylation despite protein turnover.

Conclusions:

  • A model for synaptic memory involving CaMKII is proposed.
  • The model outlines CaMKII's role from activation to sustained synaptic potentiation.
  • Further research is needed to strengthen or refine specific steps in the CaMKII-mediated memory model.