Evidence map›Paper›PMID 33804598›Full record

ArticleInternational journal of molecular sciences2021

CaMKIIα Expressing Neurons to Report Activity-Related Endogenous Hypoxia upon Motor-Cognitive Challenge.

Umer Javed Butt, Imam Hassouna, Laura Fernandez Garcia-Agudo, Agnes A Steixner-Kumar, Constanze Depp, Nadine Barnkothe, Matthias R Zillmann, Anja Ronnenberg, Viktoria Bonet, Sandra Goebbels and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Neuronal and Brain Maturation.International journal of molecular sciences · 2022
    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

12 authors.

Umer Javed ButtClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Imam HassounaClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Laura Fernandez Garcia-AgudoClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Agnes A Steixner-KumarClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.ORCID 0000-0001-7913-2716
Constanze DeppDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Nadine BarnkotheClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Matthias R ZillmannClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.ORCID 0000-0002-4222-0947
Anja RonnenbergClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Viktoria BonetClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Sandra GoebbelsDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Hannelore EhrenreichClinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.ORCID 0000-0001-8371-5711

Funding

German Research Foundation (DFG) TRR 274/1 2020 - 408885537
6 · The paper itself

Abstract

We previously introduced the brain erythropoietin (EPO) circle as a model to explain the adaptive 'brain hardware upgrade' and enhanced performance. In this fundamental circle, brain cells, challenged by motor-cognitive tasks, experience functional hypoxia, triggering the expression of EPO among other genes. We attested hypoxic cells by a transgenic reporter approach under the ubiquitous CAG promoter, with Hif-1α oxygen-dependent degradation-domain (ODD) fused to CreERT2-recombinase. To specifically focus on the functional hypoxia of excitatory pyramidal neurons, here, we generated CaMKIIα-CreERT2-ODD::R26R-tdTomato mice. Behavioral challenges, light-sheet microscopy, immunohistochemistry, single-cell mRNA-seq, and neuronal cultures under normoxia or hypoxia served to portray these mice. Upon complex running wheel performance as the motor-cognitive task, a distinct increase in functional hypoxic neurons was assessed immunohistochemically and confirmed three-dimensionally. In contrast, fear conditioning as hippocampal stimulus was likely too short-lived to provoke neuronal hypoxia. Transcriptome data of hippocampus under normoxia versus inspiratory hypoxia revealed increases in CA1 CaMKIIα-neurons with an immature signature, characterized by the expression of

Indexed as

CognitionGene ExpressionAnimalsBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell HypoxiaCells, CulturedComputational BiologyDose-Response Relationship, DrugDoublecortin ProteinFluorescent Antibody TechniqueGene Expression ProfilingGenes, ReporterHypoxiaImmunohistochemistryMiceCalcium-Calmodulin-Dependent Protein Kinase Type 2Dcx protein, mouseDoublecortin ProteinTamoxifenbrain maturationcomplex running wheelHif-1αhippocampusimmature neuronslight-sheet microscopyneuronal differentiationneuron culturephysiological hypoxiascRNA-seq

Identifiers

PMID33804598
PMCPMC8003772

What Socratic holds

Textmetadata
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 Socratic graph.