Evidence map›Paper›PMID 25276438›Full record

ArticleNeural plasticity2014

Abeta(1-42) enhances neuronal excitability in the CA1 via NR2B subunit-containing NMDA receptors.

Edina Varga, Gábor Juhász, Zsolt Bozsó, Botond Penke, Lívia Fülöp, Viktor Szegedi

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Dual Role of NMDAR Containing NR2A and NR2B Subunits in Alzheimer's Disease.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Role of Aβ in Alzheimer's-related synaptic dysfunction.Frontiers in cell and developmental biology · 2022
    Review
  6. Article
  7. Article
  8. Alterations in GABAFrontiers in cellular neuroscience · 2019
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. TRPA1 channels promote astrocytic CaMolecular neurodegeneration · 2017
    Article
  14. 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

6 authors at 2 institutions in 1 country.

Edina VargaDepartment of Medical Chemistry, University of Szeged, Szeged 6726, Hungary.ORCID 0000-0002-4193-8383
Gábor JuhászDepartment of Medical Chemistry, University of Szeged, Szeged 6726, Hungary.ORCID 0000-0001-6912-5109
Zsolt BozsóDepartment of Medical Chemistry, University of Szeged, Szeged 6726, Hungary.
Botond PenkeDepartment of Medical Chemistry, University of Szeged, Szeged 6726, Hungary.
Lívia FülöpDepartment of Medical Chemistry, University of Szeged, Szeged 6726, Hungary.
Viktor SzegediBiological Research Center-Biochemistry, Hungarian Academy of Sciences, Temesvari Körút 32, Szeged 6726, Hungary.ORCID 0000-0003-4191-379X
University of Szeged · HUHungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal hyperexcitability is a phenomenon associated with early Alzheimer's disease. The underlying mechanism is considered to involve excessive activation of glutamate receptors; however, the exact molecular pathway remains to be determined. Extracellular recording from the CA1 of hippocampal slices is a long-standing standard for a range of studies both in basic research and in neuropharmacology. Evoked field potentials (fEPSPs) are regarded as the input, while spiking rate is regarded as the output of the neuronal network; however, the relationship between these two phenomena is not fully clear. We investigated the relationship between spontaneous spiking and evoked fEPSPs using mouse hippocampal slices. Blocking AMPA receptors (AMPARs) with CNQX abolished fEPSPs, but left firing rate unchanged. NMDA receptor (NMDAR) blockade with MK801 decreased neuronal spiking dose dependently without altering fEPSPs. Activating NMDARs by small concentration of NMDA induced a trend of increased firing. These results suggest that fEPSPs are mediated by synaptic activation of AMPARs, while spontaneous firing is regulated by the activation of extrasynaptic NMDARs. Synaptotoxic Abeta(1-42) increased firing activity without modifying evoked fEPSPs. This hyperexcitation was prevented by ifenprodil, an antagonist of the NR2B NMDARs. Overall, these results suggest that Abeta(1-42) induced neuronal overactivity is not dependent on AMPARs but requires NR2B.

Indexed as

Action PotentialsAmyloid beta-PeptidesAnimalsCA1 Region, HippocampalExcitatory Postsynaptic PotentialsLong-Term PotentiationMiceMice, Inbred BALB CNeuronsPeptide FragmentsReceptors, AMPAReceptors, N-Methyl-D-AspartateAmyloid beta-Peptidesamyloid beta-protein (1-42)NR2B NMDA receptorPeptide FragmentsReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25276438
PMCPMC4168240
OpenAlexW1988942178

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.