NIH R01 · 2025
CaMKII holoenzyme mechanisms in opposing forms of synaptic plasticity
Project Summary/Abstract Stimulation of hippocampal NMDA-type glutamate receptors (NMDARs) can induce long-term potentiation (LTP) or depression (LTD), two opposing forms of synaptic plasticity that are thought to be required for higher brain functions such as learning, memory and cognition. This proposal will focus on the molecular computation that mediates the decision between these two forms of plasticity. LTP has long been known to require the Ca2+/calmodulin(CaM)-dependent protein kinase II (CaMKII) and its autophosphorylation at T286 (pT286), which generates Ca2+-independent “autonomous” CaMKII activity (~20% of the maximal Ca2+/CaM-stimulated activity). In the first funding period of…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.