Evidence map›Paper›PMID 19666491›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Regional differences in hippocampal calcium handling provide a cellular mechanism for limiting plasticity.

Stephen B Simons, Yasmin Escobedo, Ryohei Yasuda, Serena M Dudek

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

75 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. All-optical mapping of CaCell calcium · 2025
    Article
  15. Identification of hippocampal area CA2 in hamster and vole brain.The Journal of comparative neurology · 2024
    Article
  16. Article
  17. Identification of hippocampal area CA2 in hamster and vole brain.bioRxiv : the preprint server for biology · 2024
    Article
  18. Review
  19. Article
  20. Article

15 more citing papers are in PubMed but not listed here.

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.

Stephen B SimonsLaboratory of Neurobiology, Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Yasmin Escobedo
Ryohei Yasuda
Serena M Dudek
Duke Medical Center · USNational Institute of Environmental Health Sciences · US

Funding

Mechanisms Of Synaptic Plasticity In The Adult And Developing Nervous SystemZIAES100221 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI DUDEK, SERENA M · 2009 to 2025
$47.4M
Mechanisms of Ras Signaling in Single SynapsesR01MH080047 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2007 to 2023
$6.8M
NIMH NIH HHS R01 MH080047NIMH NIH HHS R01MH080047
6 · The paper itself

Abstract

Although much is known about the mechanisms underlying synaptic plasticity, the cellular mechanisms that negatively regulate plasticity in some brain regions are considerably less studied. One region where neurons do not reliably express long-term potentiation (LTP) is the CA2 subfield of the hippocampus. Given the connection between synaptic plasticity and increases in postsynaptic [Ca(2+)], and that CA2 neurons express a large number of calcium-regulating proteins, we tested the hypothesis that the relative lack of LTP in CA2 results from differences in the calcium dynamics of these neurons. By measuring calcium-dependent fluorescence transients in dendritic spines, we show that CA2 neurons have smaller action potential-evoked intracellular Ca(2+) transients because of a higher endogenous Ca(2+)-buffering capacity and significantly higher rates of Ca(2+) extrusion when compared with CA1 and CA3 neurons. Perfusion with higher external [Ca(2+)] during induction restores LTP to CA2 neurons, suggesting that they possess the cellular machinery required for plasticity, but that the restriction of postsynaptic [Ca(2+)] limits its expression. Camstatin, an analogue of the calcium-modulating protein Pep-19 strongly expressed in CA2 neurons, blocked LTP and increased Ca(2+) extrusion in CA1 neurons, suggesting a role for extrusion in the regulation of plasticity in CA2. In agreement with this idea, we found that intracellular introduction of a PMCA pump inhibitor (carboxyeosin) allows for the induction of LTP in CA2 neurons. Our results indicate that regulation of postsynaptic [Ca(2+)] through modulation of extrusion and/or buffering regulates expression of LTP in CA2 and potentially other brain regions.

Indexed as

AnimalsCalciumCalcium SignalingDendritesElectrophysiologyEosine Yellowish-(YS)HippocampusKineticsMicroscopy, FluorescenceModels, BiologicalNeuronal PlasticityNeuronsRatsSynaptic TransmissionCalciumEosine Yellowish-(YS)

Identifiers

PMID19666491
PMCPMC2729023
OpenAlexW2034513993

What OpenQuestion holds

Textmetadata
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.