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Cited by 16Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeural dynamics and brain function

Long-term potentiation can be induced in the CA1 region of hippocampus in the absence of αCaMKII T286-autophosphorylation

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Villers, Agnès, Giese, Karl Peter, Ris, Laurence·2014·Learning & Memory
DOI 10.1101/lm.035972.114PMC PMC4201817
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Abstract

α-calcium/calmodulin-dependent protein kinase (αCaMKII) T286-autophosphorylation provides a short-term molecular memory that was thought to be required for LTP and for learning and memory. However, it has been shown that learning can occur in αCaMKII-T286A mutant mice after a massed training protocol. This raises the question of whether there might be a form of LTP in these mice that can occur without T286 autophosphorylation. In this study, we confirmed that in CA1 pyramidal cells, LTP induced in acute hippocampal slices, after a recovery period in an interface chamber, is strictly dependent on postsynaptic αCaMKII autophosphorylation. However, we demonstrated that αCaMKII-autophosphorylation-independent plasticity can occur in the hippocampus but at the expense of synaptic specificity. This nonspecific LTP was observed in mutant and wild-type mice after a recovery period in a submersion chamber and was independent of NMDA receptors. Moreover, when slices prepared from mutant mice were preincubated during 2 h with rapamycin, high-frequency trains induced a synapse-specific LTP which was added to the nonspecific LTP. This specific LTP was related to an increase in the duration and the amplitude of NMDA receptor-mediated response induced by rapamycin.

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  • NMDAR-dependent LTP is greatly impaired when T286 is replaced by T286A.

    “Foremost are data, now long accepted, that NMDAR-dependent LTP is greatly impaired when T286 is replaced by T286A (43, 121, 381–384).”

    From Synaptic memory and CaMKII (2023) · cites this paper as [382]

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Authors
Villers, A., Giese, K. P., & Ris, L.
Affiliations
  • University of Mons (BE)
  • King's College London (GB)
Corresponding author
Ris, Laurence
ORCID
Venue
Learning & Memory
Publisher
Cold Spring Harbor Laboratory
Published
2014-10-16
Volume
21
Issue
11
Pages
616-626
ISSN
  • 1072-0502 (ISSN-L)
  • 1549-5485
DOI
10.1101/lm.035972.114
PMC
PMC4201817
OpenAlex
W2016458636
Cited by
16
References
16
Citations by year
2025: 1 · 2023: 3 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 3 · 2015: 1
Type
posted content
Language
en
Open access
Licence
cc-by-nc
Locations
  • Learning & Memory (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (submittedVersion)
  • HighWire Press Open Archive (submittedVersion, cc-by-nc)
  • ORBi UMONS (submittedVersion)
Funders
  • Belgian Queen Elisabeth Medical Foundation
  • Belgian Fund for Scientific Research
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
long-term potentiation, CaMKIIα, CA1 pyramidal neurons, hippocampus, NMDA receptor, rapamycin, mTOR signaling, learning and memory
MeSH terms
Animals, Mice, Inbred C57BL, Phosphorylation, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Pyramidal Cells, Sirolimus, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2, CA1 Region, Hippocampal, TOR Serine-Threonine Kinases

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