Cited by 425Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsTreatment of Major Depression

Long-Term Potentiation: From CaMKII to AMPA Receptor Trafficking

Herring, Bruce E., Nicoll, Roger A.·2016·Annual Review of Physiology

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.

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Crossref · 10.1146/annurev-physiol-021014-071753

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18 of 18 references verified0 citation errors · 0 not checkable

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  • Kalirin and Trio serve critical and functionally redundant roles in supporting excitatory synapse structure and function.

    “Kalirin and Trio serve critical and functionally redundant roles in supporting excitatory synapse structure and function (32, 318).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [32]

  • There is compelling evidence that CaMKII, via phosphorylation, initiates a series of actin-based cytoskeletal rearrangements in the spine.

    “Indeed, there is compelling evidence that CaMKII, via phosphorylation, initiates a series of actin-based cytoskeletal rearrangements in the spine (32, 312–314).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [32]

  • NMDAR-dependent LTP is the result of increased AMPAR density in the post-synaptic membrane and/or single channel conductance of the AMPAR.

    “The major form of LTP identified in the brain, NMDAR-dependent LTP, is the result of increased AMPAR density in the post-synaptic membrane and/or single channel conductance of the AMPAR (Huganir and Nicoll, 2013, Herring and Nicoll, 2016, Poncer et al., 2002, Benke et al., 1998).”

    From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Herring and Nicoll, 2016

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Authors
Herring, B. E., & Nicoll, R. A.
Affiliations
  • Department of Cellular and Molecular Pharmacology and
  • University of California, San Francisco (US)
Venue
Annual Review of Physiology
Published
2016-02-10
Volume
78
Issue
1
Pages
351-365
ISSN
  • 0066-4278 (ISSN-L)
  • 1545-1585
OpenAlex
W2157702984
Cited by
425
References
18
Citations by year
2026: 16 · 2025: 28 · 2024: 33 · 2023: 49 · 2022: 43 · 2021: 57 · 2020: 55 · 2019: 37 · 2018: 59 · 2017: 33 · 2016: 13 · 2014: 1
FWCI
5.18
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (R01MH070957)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
long-term potentiation, CaMKII, AMPA receptor trafficking, synaptic plasticity, calcium/calmodulin-dependent protein kinase
MeSH terms
Animals, Humans, Long-Term Potentiation, Receptors, AMPA, Protein Transport, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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