Evidence map›Paper›PMID 27848967›Full record

ArticleNature communications2016

Dendritic NMDA spikes are necessary for timing-dependent associative LTP in CA3 pyramidal cells.

Federico Brandalise, Stefano Carta, Fritjof Helmchen, John Lisman, Urs Gerber

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 110 citations in OpenAlex.

  1. Distinct types of dendritic CaScience advances · 2026
    Article
  2. Article
  3. Robust input disentanglement through dendritic calcium-mediated action potentials.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Astrocytic CaNature neuroscience · 2025
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
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  13. Cholinergic regulation of dendritic CaProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Heterosynaptic plasticity-induced modulation of synapses.The journal of physiological sciences : JPS · 2023
    Review
  19. Review
  20. Article
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 2 institutions in 2 countries.

Federico BrandaliseBrain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.
Stefano CartaBrain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.
Fritjof HelmchenBrain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.
John LismanDepartment of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02453, USA.
Urs GerberBrain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.
University of Zurich · CHBrandeis University · US

Funding

Role of CaMKII in memory storageR01NS103168 · NINDS · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 2017 to 2021
$1.8M
Role of CaMKII in memory storageR56NS096710 · NINDS · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 2016 to 2016
$484k
NINDS NIH HHS R01 NS103168NINDS NIH HHS R56 NS096710
6 · The paper itself

Abstract

The computational repertoire of neurons is enhanced by regenerative electrical signals initiated in dendrites. These events, referred to as dendritic spikes, can act as cell-intrinsic amplifiers of synaptic input. Among these signals, dendritic NMDA spikes are of interest in light of their correlation with synaptic LTP induction. Because it is not possible to block NMDA spikes pharmacologically while maintaining NMDA receptors available to initiate synaptic plasticity, it remains unclear whether NMDA spikes alone can trigger LTP. Here we use dendritic recordings and calcium imaging to analyse the role of NMDA spikes in associative LTP in CA3 pyramidal cells. We show that NMDA spikes produce regenerative branch-specific calcium transients. Decreasing the probability of NMDA spikes reduces LTP, whereas increasing their probability enhances LTP. NMDA spikes and LTP occur without back-propagating action potentials. However, action potentials can facilitate LTP induction by promoting NMDA spikes. Thus, NMDA spikes are necessary and sufficient to produce the critical postsynaptic depolarization required for associative LTP in CA3 pyramidal cells.

Indexed as

Action PotentialsLong-Term PotentiationAnimalsCA3 Region, HippocampalCalciumDendritesNeuronal PlasticityN-MethylaspartateProbabilityPyramidal CellsRats, WistarReceptors, N-Methyl-D-AspartateSynapsesTime FactorsCalciumN-MethylaspartateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID27848967
PMCPMC5116082
OpenAlexW2555072090

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.