A revised view of the role of CaMKII in learning and memory

K Ulli Bayer, Peter Giese

Research output: Contribution to journalReview articlepeer-review

2 Citations (Scopus)

Abstract

The Ca2+/Calmodulin(CaM)-dependent protein kinase II (CaMKII) plays a fundamental role in learning and possibly also in memory. However, current mechanistic models require fundamental revision. CaMKII autophosphorylation at T286 (pT286) does not provide the molecular basis for long-term memory, as long believed. Instead, pT286 mediates the signal processing required for induction of several distinct forms of synaptic plasticity, including Hebbian long-term potentiation and depression (LTP and LTD) and non-Hebbian behavioral timescale synaptic plasticity (BTSP). We discuss (i) the molecular computations by which CaMKII supports these diverse plasticity mechanisms, (ii) alternative CaMKII mechanisms that may contribute to the maintenance phase of LTP, and (iii) the relationship of these mechanisms to behavioral learning and memory
Original languageEnglish
JournalNature neuroscience
DOIs
Publication statusPublished - 18 Nov 2024

Keywords

  • Learning, memory, synapse, signalling

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