Evidence map›Paper›PMID 26901094›Full record

ArticleEndocrinology2016

Spontaneous and CRH-Induced Excitability and Calcium Signaling in Mice Corticotrophs Involves Sodium, Calcium, and Cation-Conducting Channels.

Hana Zemkova, Melanija Tomić, Marek Kucka, Greti Aguilera, Stanko S Stojilkovic

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Fast dynamics in the HPA axis: Insight from mathematical and experimental studies.Current opinion in endocrine and metabolic research · 2022
    Review
  7. Review
  8. Article
  9. Expression and Role of Thyrotropin Receptors in Proopiomelanocortin-Producing Pituitary Cells.Thyroid : official journal of the American Thyroid Association · 2021
    Article
  10. Article
  11. Imaging of Endoplasmic Reticulum CaFrontiers in endocrinology · 2020
    Article
  12. Article
  13. Store-operated CaBiochimica et biophysica acta. Molecular cell research · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. 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.

Hana ZemkovaDepartment of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic (H.Z.); and Sections on Cellular Signaling (H.Z., M.T., M.K., S.S.S.) and Endocrine Physiology (G.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510.
Melanija TomićDepartment of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic (H.Z.); and Sections on Cellular Signaling (H.Z., M.T., M.K., S.S.S.) and Endocrine Physiology (G.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510.
Marek KuckaDepartment of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic (H.Z.); and Sections on Cellular Signaling (H.Z., M.T., M.K., S.S.S.) and Endocrine Physiology (G.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510.
Greti AguileraDepartment of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic (H.Z.); and Sections on Cellular Signaling (H.Z., M.T., M.K., S.S.S.) and Endocrine Physiology (G.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510.
Stanko S StojilkovicDepartment of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic (H.Z.); and Sections on Cellular Signaling (H.Z., M.T., M.K., S.S.S.) and Endocrine Physiology (G.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510.
Czech Academy of Sciences, Institute of Physiology · CZEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Intracellular Signaling In Endocrine CellsZIAHD000195 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STOJILKOVIC, STANKO S. · 2009 to 2025
$18.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Transgenic mice expressing the tdimer2(12) form of Discosoma red fluorescent protein under control of the proopiomelanocortin gene's regulatory elements are a useful model for studying corticotrophs. Using these mice, we studied the ion channels and mechanisms controlling corticotroph excitability. Corticotrophs were either quiescent or electrically active, with a 22-mV difference in the resting membrane potential (RMP) between the 2 groups. In quiescent cells, CRH depolarized the membrane, leading to initial single spiking and sustained bursting; in active cells, CRH further facilitated or inhibited electrical activity and calcium spiking, depending on the initial activity pattern and CRH concentration. The stimulatory but not inhibitory action of CRH on electrical activity was mimicked by cAMP independently of the presence or absence of arachidonic acid. Removal of bath sodium silenced spiking and hyperpolarized the majority of cells; in contrast, the removal of bath calcium did not affect RMP but reduced CRH-induced depolarization, which abolished bursting electrical activity and decreased the spiking frequency but not the amplitude of single spikes. Corticotrophs with inhibited voltage-gated sodium channels fired calcium-dependent action potentials, whereas cells with inhibited L-type calcium channels fired sodium-dependent spikes; blockade of both channels abolished spiking without affecting the RMP. These results indicate that the background voltage-insensitive sodium conductance influences RMP, the CRH-depolarization current is driven by a cationic conductance, and the interplay between voltage-gated sodium and calcium channels plays a critical role in determining the status and pattern of electrical activity and calcium signaling.

Indexed as

Action PotentialsAnimalsArachidonic AcidBucladesineCalciumCalcium Channels, L-TypeCalcium SignalingCells, CulturedColforsinCorticotrophsCorticotropin-Releasing HormoneCyclic AMPFemaleIon ChannelsMaleMembrane PotentialsArachidonic AcidBucladesineCalciumCalcium Channels, L-TypeColforsinCorticotropin-Releasing HormoneCyclic AMPIon ChannelsSodium

Identifiers

PMID26901094
PMCPMC4816721
OpenAlexW2284148867

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.