Evidence map›Paper›PMID 37672577›Full record

ArticleScience advances2023

A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons.

Kuo Xiao, Yiding Li, Raymond A Chitwood, Jeffrey C Magee

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Dendritic Inhibition Terminates Plateau Potentials in CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Behavioral Timescale Synaptic Plasticity: A Burst in the Field of Learning and Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Review
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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

4 authors at 2 institutions in 1 country.

Kuo XiaoDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0001-6112-9930
Yiding LiDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0002-5176-0814
Raymond A ChitwoodDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0002-2016-5238
Jeffrey C MageeDepartment of Neuroscience, Baylor College of Medicine, Houston, TX, USA.ORCID 0000-0002-1299-9347
Howard Hughes Medical Institute · USBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Behavioral timescale synaptic plasticity (BTSP) is a type of non-Hebbian synaptic plasticity reported to underlie place field formation. Despite this important function, the molecular mechanisms underlying BTSP are poorly understood. The α-calcium-calmodulin-dependent protein kinase II (αCaMKII) is activated by synaptic transmission-mediated calcium influx, and its subsequent phosphorylation is central to synaptic plasticity. Because the activity of αCaMKII is known to outlast the event triggering phosphorylation, we hypothesized that it could mediate the extended timescale of BTSP. To examine the role of αCaMKII in BTSP, we performed whole-cell in vivo and in vitro recordings in CA1 pyramidal neurons from mice engineered with a point mutation at the autophosphorylation site (T286A) causing accelerated signaling kinetics. Here, we demonstrate a profound deficit in synaptic plasticity, strongly suggesting that αCaMKII signaling is required for BTSP. This study elucidates part of the molecular mechanism of BTSP and provides insight into the function of αCaMKII in place cell formation and ultimately learning and memory.

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2Pyramidal CellsAnimalsHippocampusKineticsMiceNeuronal PlasticityCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouse

Identifiers

PMID37672577
PMCPMC10482326
OpenAlexW4386474186

What OpenQuestion holds

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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.