| Literature DB >> 26863325 |
Bruce E Herring1, Roger A Nicoll1,2.
Abstract
For more than 20 years, we have known that Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation is both necessary and sufficient for the induction of long-term potentiation (LTP). During this time, tremendous effort has been spent in attempting to understand how CaMKII activation gives rise to this phenomenon. Despite such efforts, there is much to be learned about the molecular mechanisms involved in LTP induction downstream of CaMKII activation. In this review, we highlight recent developments that have shaped our current thinking about the molecular mechanisms underlying LTP and discuss important questions that remain in the field.Entities:
Keywords: LTP; memory; plasticity; spine; synapse
Mesh:
Substances:
Year: 2016 PMID: 26863325 DOI: 10.1146/annurev-physiol-021014-071753
Source DB: PubMed Journal: Annu Rev Physiol ISSN: 0066-4278 Impact factor: 19.318