Evidence map›Paper›PMID 28642476›Full record

ArticleScientific reports2017

Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor.

Fabio Antonio Vigil, Keiko Mizuno, Walter Lucchesi, Victoria Valls-Comamala, Karl Peter Giese

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  7. Muscarinic receptor activation overrides boundary conditions on memory updating in a calcium/calmodulin-dependent manner.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
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  16. Molecular Mechanisms of Reconsolidation-Dependent Memory Updating.International journal of molecular sciences · 2020
    Review
  17. Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  18. Function and mechanisms of memory destabilization and reconsolidation after retrieval.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2020
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Fabio Antonio VigilDepartment of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Keiko MizunoDepartment of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Walter LucchesiDepartment of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Victoria Valls-ComamalaDepartment of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom.
Karl Peter GieseDepartment of Basic and Clinical Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, United Kingdom. karl.giese@kcl.ac.uk.
King's College London · GB

Funding

Medical Research Council G0800393
6 · The paper itself

Abstract

CaMK2N1 and CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning and memory. Here, we investigated the learning and memory function of CaMK2N1 by knocking-down its expression in dorsal hippocampus of mice. We found that reduced CaMK2N1 expression does not affect contextual fear long-term memory (LTM) formation. However, we show that it impairs maintenance of established LTM, but only if retrieval occurs. CaMK2N1 knockdown prevents a decrease of threonine-286 (T286) autophosphorylation of αCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear LTM. CaMK2N1 knockdown can also increase CaMK2N2 expression, but we show that such increased expression does not affect LTM after retrieval. We also found that substantial overexpression of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not required for LTM storage. Taken together, we propose a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autophosphorylation of αCaMKII.

Indexed as

Memory, Long-TermAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Carrier ProteinsFearGene ExpressionGene Knockdown TechniquesHippocampusIntracellular Signaling Peptides and ProteinsMaleMicePhosphorylationReceptors, AMPARNA InterferenceRNA, MessengerRNA, Small InterferingCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2n2 protein, mouseCarrier ProteinsIntracellular Signaling Peptides and ProteinsReceptors, AMPARNA, MessengerRNA, Small Interfering

Identifiers

PMID28642476
PMCPMC5481336
OpenAlexW2625037436

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.