Evidence map›Paper›PMID 38077336›Full record

ArticleFrontiers in immunology2023

A

Marina Wendlandt, Alina J Kürten, Antonia Beiersdorfer, Charlotte Schubert, Kiana Samad-Yazdtchi, Jessica Sauer, M Carolina Pinto, Kristina Schulz, Manuel A Friese, Christine E Gee and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Developmental changes in CaScientific reports · 2026
    Article
  3. Crosstalk of noradrenergic CaCell communication and signaling : CCS · 2026
    Article
  4. 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 at 2 institutions in 1 country.

Marina WendlandtDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Alina J KürtenDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Antonia BeiersdorferDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Charlotte SchubertInstitute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kiana Samad-YazdtchiDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Jessica SauerDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
M Carolina PintoInstitute of Synaptic Physiology, Center for Molecular Neurobiology Hamburg, Hamburg, Germany.
Kristina SchulzDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Manuel A FrieseInstitute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Christine E GeeInstitute of Synaptic Physiology, Center for Molecular Neurobiology Hamburg, Hamburg, Germany.
Daniela HirnetDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Christian LohrDivision of Neurophysiology, University of Hamburg, Hamburg, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The cyclic nucleotide cyclic adenosine monophosphate (cAMP) is a ubiquitous second messenger, which is known to play an important anti-inflammatory role. Astrocytes in the central nervous system (CNS) can modulate inflammation but little is known about the significance of cAMP in their function. Methods: We investigated cAMP dynamics in mouse olfactory bulb astrocytes in brain slices prepared from healthy and experimental autoimmune encephalomyelitis (EAE) mice. Results: The purinergic receptor ligands adenosine and adenosine triphosphate (ATP) both induced transient increases in cAMP in astrocytes expressing the genetically encoded cAMP sensor Flamindo2. The A Discussion: Our results indicate that ATP, synaptically released by afferent axons in the olfactory bulb, is degraded to adenosine that acts on A

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalAdenosineAdenosine TriphosphateAnimalsAstrocytesCyclic AMPMiceOlfactory BulbReceptors, Purinergic P1AdenosineAdenosine TriphosphateCyclic AMPReceptors, Purinergic P1adenosineastrocytecAMP imagingcyclic adenosine monophosphateexperimental autoimmune encephalomyelitisneuroinflammationolfactory bulbpurinergic signaling

Identifiers

PMID38077336
PMCPMC10701430
OpenAlexW4388944839

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.