Evidence map›Paper›PMID 21371490›Full record

ArticleSteroids2011

Progesterone inhibition of voltage-gated calcium channels is a potential neuroprotective mechanism against excitotoxicity.

Jessie I Luoma, Brooke G Kelley, Paul G Mermelstein

Abstract read
In one paragraph

Article in Steroids, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Progesterone for acute traumatic brain injury.The Cochrane database of systematic reviews · 2016
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. The Effects of Neuroactive Steroids on Myelin in Health and Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Quercetin's Effects on Glutamate Cytotoxicity.Molecules (Basel, Switzerland) · 2022
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Aging GABAergic System and Its Nutritional Support.Journal of nutrition and metabolism · 2021
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Jessie I LuomaDepartment of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. luom0025@umn.edu
Brooke G Kelley
Paul G Mermelstein
University of Minnesota · US

Funding

Novel Actions of Estradiol that Influence Brain FunctionR01NS041302 · NINDS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MERMELSTEIN, PAUL G · 2001 to 2010
$2.5M
Postdoctoral Training Program in Duluth, MinnesotaK12GM074628 · NIGMS · UNIVERSITY OF MINNESOTA · PI TRACHTE, GEORGE J · 2007 to 2011
$1.5M
NIGMS NIH HHS GM074628NIGMS NIH HHS K12 GM074628NINDS NIH HHS NS41302NINDS NIH HHS R01 NS041302
6 · The paper itself

Abstract

The therapeutic use of progesterone following traumatic brain injury has recently entered phase III clinical trials as a means of neuroprotection. Although it has been hypothesized that progesterone protects against calcium overload following excitotoxic shock, the exact mechanisms underlying the beneficial effects of progesterone have yet to be determined. We found that therapeutic concentrations of progesterone to be neuroprotective against depolarization-induced excitotoxicity in cultured striatal neurons. Through use of calcium imaging, electrophysiology and the measurement of changes in activity-dependent gene expression, progesterone was found to block calcium entry through voltage-gated calcium channels, leading to alterations in the signaling of the activity-dependent transcription factors NFAT and CREB. The effects of progesterone were highly specific to this steroid hormone, although they did not appear to be receptor mediated. In addition, progesterone did not inhibit AMPA or NMDA receptor signaling. This analysis regarding the effect of progesterone on calcium signaling provides both a putative mechanism by which progesterone acts as a neuroprotectant, as well as affords a greater appreciation for its potential far-reaching effects on cellular function.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dionealpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsApoptosisBrainBrain InjuriesCalcium Channel BlockersCalcium Channels, L-TypeCalcium SignalingCells, CulturedCyclic AMP Response Element-Binding ProteinExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsFemaleGene ExpressionGenes, Reporter6-Cyano-7-nitroquinoxaline-2,3-dionealpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidCalcium Channel BlockersCalcium Channels, L-TypeCyclic AMP Response Element-Binding ProteinExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsGlutamic AcidLuciferasesNeuroprotective AgentsNFATC Transcription FactorsNifedipineN-MethylaspartatePotassiumProgesterone

Identifiers

PMID21371490
PMCPMC3129396
OpenAlexW1967370689

What OpenQuestion holds

Textmetadata
LicenceTDM
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.