Evidence map›Paper›PMID 18339621›Full record

ArticleThe Journal of biological chemistry2008

Ablation of Ca2+ channel beta3 subunit leads to enhanced N-methyl-D-aspartate receptor-dependent long term potentiation and improved long term memory.

Daejong Jeon, Inseon Song, William Guido, Karam Kim, Eunjoon Kim, Uhtaek Oh, Hee-Sup Shin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cavβ3 Regulates CaDiabetes · 2021
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Blocking CaCell reports · 2018
    Article
  11. Two Components of Aversive Memory inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  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

7 authors at 4 institutions in 3 countries.

Daejong JeonCenter for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea.
Inseon Song
William Guido
Karam Kim
Eunjoon Kim
Uhtaek Oh
Hee-Sup Shin
Korea Institute of Science and Technology · KRKorea Advanced Institute of Science and Technology · KRSeoul National University · KRVirginia Commonwealth University Medical Center · US

Funding

FUNCTIONAL STATE OF DEVELOPING RETINOGENICULATE SYNAPSER01EY012716 · NEI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GUIDO, WILLIAM · 2001 to 2021
$6.9M
NEI NIH HHS EY12716NEI NIH HHS R01 EY012716
6 · The paper itself

Abstract

The beta subunits of voltage-dependent Ca(2+) channels (VDCCs) have marked effects on the properties of the pore-forming alpha(1) subunits of VDCCs, including surface expression of channel complexes and modification of voltage-dependent kinetics. Among the four different beta subunits, the beta(3) subunit (Ca(v)beta3) is abundantly expressed in the hippocampus. However, the role of Ca(v)beta3 in hippocampal physiology and function in vivo has never been examined. Here, we investigated Ca(v)beta3-deficient mice for hippocampus-dependent learning and memory and synaptic plasticity at hippocampal CA3-CA1 synapses. Interestingly, the mutant mice exhibited enhanced performance in several hippocampus-dependent learning and memory tasks. However, electrophysiological studies revealed no alteration in the Ca(2+) current density, the frequency and amplitude of miniature excitatory postsynaptic currents, and the basal synaptic transmission in the mutant hippocampus. On the other hand, however, N-methyl-d-aspartate receptor (NMDAR)-mediated synaptic currents and NMDAR-dependent long term potentiation were significantly increased in the mutant. Protein blot analysis showed a slight increase in the level of NMDAR-2B in the mutant hippocampus. Our results suggest a possibility that, unrelated to VDCCs regulation, Ca(v)beta3 negatively regulates the NMDAR activity in the hippocampus and thus activity-dependent synaptic plasticity and cognitive behaviors in the mouse.

Indexed as

AnimalsCalcium Channels, L-TypeFearFood PreferencesHippocampusIon Channel GatingLong-Term PotentiationMembrane PotentialsMemoryMiceMice, Inbred C57BLProtein SubunitsPyramidal CellsReceptors, N-Methyl-D-AspartateRecognition, PsychologySynaptic TransmissionCalcium Channels, L-TypeNR2B NMDA receptorProtein SubunitsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID18339621
PMCPMC3774114
OpenAlexW2115399420

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.