A Revised View of the Role of CaMKII in Learning and Memory
Overview
Authors
Affiliations
The Ca/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 Thr286 (pThr286) does not provide the molecular basis for long-term memory, as long believed. Instead, pThr286 mediates the signal processing required for induction of several distinct forms of synaptic plasticity, including Hebbian long-term potentiation and depression and non-Hebbian behavioral timescale synaptic plasticity. 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.
Enhancing Retinal Resilience: The Neuroprotective Promise of BDNF in Diabetic Retinopathy.
Tanase D, Valasciuc E, Gosav E, Floria M, Buliga-Finis O, Ouatu A Life (Basel). 2025; 15(2).
PMID: 40003672 PMC: 11856995. DOI: 10.3390/life15020263.