Related Experiment Video
Updated: May 24, 2026

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
Published on: June 26, 2013
Mechanisms of CaMKII action in long-term potentiation
John Lisman1, Ryohei Yasuda, Sridhar Raghavachari
1Department of Biology, Brandeis University, Waltham, Massachusetts 02454, USA. lisman@brandeis.edu
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.
Related Concept Videos
Long-term Potentiation
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Long-term Depression
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression
cAMP-dependent Protein Kinase Pathways

