LTP expression mediated by autonomous activity of GluN2B-bound CaMKII.

ABSTRACT: Learning and memory are thought to require the induction and maintenance of long-term potentiation (LTP) of synaptic strength. LTP induction requires the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) but for structural rather than enzymatic functions. We show that the relevant structural function is regulated by CaMKII binding to the NMDA-type glutamate receptor subunit GluN2B. This binding directly generates Ca²⁺-independent autonomous CaMKII activity, and we show that this enzymatic activity is dispensable for LTP induction (within 5 min) but required for a subsequent LTP phase (within 15 min). This requirement for CaMKII activity provides an objective temporal definition for the intermediary phase of LTP expression. Later LTP maintenance may still require st

SUBMITTER: Rumian NL 

PROVIDER: S-EPMC11563194 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature