There have been recent advances in understanding the molecular basis of the long-term potentiation (LTP) of synaptic transmission in the hippocampus. This review documents current views on mechanisms underlying LTP induction, from activation of the NMDA receptor to stimulation of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II). We will focus in particular on recent findings of how CaM kinase II encodes the frequency of synaptic usage and serves as a molecular memory switch at the synapse. Furthermore, a role for CaM kinase II in spatial learning and memory is demonstrated by recent studies using transgenic mice.
- Ca/calmodulin-dependent protein kinase II
- Long-term depression
- Long-term potentiation
- Spatial learning
ASJC Scopus subject areas