Evidence map›Paper›PMID 15659591›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Endogenous Ca2+ buffer concentration and Ca2+ microdomains in hippocampal neurons.

Andreas Müller, Maria Kukley, Pia Stausberg, Heinz Beck, Wolfgang Müller, Dirk Dietrich

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

72 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Modeling traveling calcium waves in cellular structures.Journal of computational neuroscience · 2025
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  12. Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  13. Article
  14. Cytosolic CaCold Spring Harbor perspectives in biology · 2020
    Review
  15. Article
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  17. Review
  18. Article
  19. Article
  20. Biphasic Modulation of NMDA Receptor Function by Metabotropic Glutamate Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article

12 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

6 authors at 1 institution in 1 country.

Andreas MüllerDepartment of Neurosurgery, University Clinic Bonn, D-53105 Bonn, Germany.
Maria Kukley
Pia Stausberg
Heinz Beck
Wolfgang Müller
Dirk Dietrich
University Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca2+-binding proteins are ubiquitously expressed throughout the CNS and serve as valuable immunohistochemical markers for certain types of neurons. However, the functional role of most Ca2+-binding proteins has to date remained obscure because their concentration in central neurons is not known. In this study, we investigate the intracellular concentration of the widely expressed Ca2+-binding protein calbindin-D28k in adult hippocampal slices using patch-clamp recordings and immunohistochemistry. First, we show that calbindin-D28k freely exchanges between patch pipette and cytoplasm during whole cell patch-clamp recordings with a time constant of approximately 10 min. Substituting known concentrations of recombinant calbindin-D28k in patch pipettes enabled us to determine the endogenous calbindin-D28k concentration by postrecording immunohistochemistry. Using this calibration procedure, we find that mature granule cells (doublecortin-) contain approximately 40 microm, and newborn granule cells (doublecortin+) contain 0-20 microm calbindin-D28k. CA3 stratum radiatum interneurons and CA1 pyramidal cells enclose approximately 47 and approximately 45 microm calbindin-D28k, respectively. Numerical simulations showed that 40 microm calbindin-D28k is capable of tuning Ca2+ microdomains associated with action potentials at the mouth of single or clustered Ca2+ channels: calbindin-D28k reduces the increment in free Ca2+ at a distance of 100 and 200 nm by 20 and 35%, respectively, and strongly accelerates the collapse of the Ca2+ gradient after cessation of Ca2+ influx. These data suggest that calbindin-D28k equips hippocampal neurons with approximately 160 microm mobile, high-affinity Ca2+-binding sites (kappa(S) approximately 200) that slow and reduce global Ca2+ signals while they enhance the spatiotemporal fidelity of submicroscopic Ca2+ signals.

Indexed as

AgingAnimalsCalbindin 1CalbindinsCalciumCalcium ChannelsCalcium SignalingDialysisDoublecortin ProteinFluorescent Antibody TechniqueHippocampusInterneuronsIn Vitro TechniquesMiceMice, KnockoutModels, BiologicalCalb1 protein, mouseCalb1 protein, ratCalbindin 1CalbindinsCalciumCalcium ChannelsDcx protein, ratDoublecortin ProteinNerve Tissue ProteinsS100 Calcium Binding Protein G

Identifiers

PMID15659591
PMCPMC6725329
OpenAlexW1967794679

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.