Excitatory postsynaptic potential

Synaptic fatigue

Neuroscience

Receptor

Dendritic spine

Biology

Synaptic augmentation

Synapse

Synaptic scaling

Hippocampal formation

Inhibitory postsynaptic potential

Neuronal memory allocation

Chemistry

Metaplasticity

Long-term potentiation

Nonsynaptic plasticity

Homosynaptic plasticity

Cell biology

Synaptic plasticity

Biochemistry

Nature reviews. Neuroscience

Calcium–calmodulin (CaM)-dependent protein kinase II (CaMKII) is the most abundant protein in excitatory synapses and is central to synaptic plasticity, learning and memory. It is activated by intracellular increases in calcium ion levels and triggers molecular processes necessary for synaptic plasticity. CaMKII phosphorylates numerous synaptic proteins, thereby regulating their structure and functions. This leads to molecular events crucial for synaptic plasticity, such as receptor trafficking, localization and activity; actin cytoskeletal dynamics; translation; and even transcription through synapse–nucleus shuttling. Several new tools affording increasingly greater spatiotemporal resolution have revealed the link between CaMKII activity and downstream signalling processes in dendritic spines during synaptic and behavioural plasticity. These technologies have provided insights into the function of CaMKII in learning and memory. Calcium–calmodulin (CaM)-dependent protein kinase II (CaMKII) has a central role in synaptic plasticity, learning and memory. In this Review, Yasuda, Hayashi and Hell provide an overview of the postsynaptic regulation and function of CaMKII.

CaMKII: a central molecular organizer of synaptic plasticity, learning and memory