Evidence map›Paper›PMID 24667541›Full record

ArticlePloS one2014

Platelet serotonin transporter function predicts default-mode network activity.

Christian Scharinger, Ulrich Rabl, Christian H Kasess, Bernhard M Meyer, Tina Hofmaier, Kersten Diers, Lucie Bartova, Gerald Pail, Wolfgang Huf, Zeljko Uzelac and 15 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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  12. Decreased mean platelet volume in panic disorder.Neuropsychiatric disease and treatment · 2014
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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

25 authors at 3 institutions in 2 countries.

Christian ScharingerDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Ulrich RablDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Christian H KasessDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria; Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria.
Bernhard M MeyerDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Tina HofmaierDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria; Center for Biomolecular Medicine and Pharmacology, Medical University of Vienna, Vienna, Austria.
Kersten DiersDepartment of Psychology, Dresden University of Technology, Dresden, Germany.
Lucie BartovaDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Gerald PailDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Wolfgang HufDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria; Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria; Department of Statistics and Probability Theory, Vienna University of Technology, Vienna, Austria.
Zeljko UzelacCenter for Biomolecular Medicine and Pharmacology, Medical University of Vienna, Vienna, Austria.
Beate HartingerDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Klaudius KalcherDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria; Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria; Department of Statistics and Probability Theory, Vienna University of Technology, Vienna, Austria.
Thomas PerkmannDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Helmuth HaslacherDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Andreas Meyer-LindenbergCentral Institute of Mental Health, University of Heidelberg, Mannheim, Germany.
Siegfried KasperDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Michael FreissmuthCenter for Biomolecular Medicine and Pharmacology, Medical University of Vienna, Vienna, Austria.
Christian WindischbergerCenter for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria.
Matthäus WilleitDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Rupert LanzenbergerDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Harald EsterbauerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Burkhard BrockeDepartment of Psychology, Dresden University of Technology, Dresden, Germany.
Ewald MoserCenter for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria.
Harald H SitteCenter for Biomolecular Medicine and Pharmacology, Medical University of Vienna, Vienna, Austria.
Lukas PezawasDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATTU Dresden · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe serotonin transporter (5-HTT) is abundantly expressed in humans by the serotonin transporter gene SLC6A4 and removes serotonin (5-HT) from extracellular space. A blood-brain relationship between platelet and synaptosomal 5-HT reuptake has been suggested, but it is unknown today, if platelet 5-HT uptake can predict neural activation of human brain networks that are known to be under serotonergic influence.

methodsA functional magnetic resonance study was performed in 48 healthy subjects and maximal 5-HT uptake velocity (Vmax) was assessed in blood platelets. We used a mixed-effects multilevel analysis technique (MEMA) to test for linear relationships between whole-brain, blood-oxygen-level dependent (BOLD) activity and platelet Vmax.

resultsThe present study demonstrates that increases in platelet Vmax significantly predict default-mode network (DMN) suppression in healthy subjects independent of genetic variation within SLC6A4. Furthermore, functional connectivity analyses indicate that platelet Vmax is related to global DMN activation and not intrinsic DMN connectivity.

conclusionThis study provides evidence that platelet Vmax predicts global DMN activation changes in healthy subjects. Given previous reports on platelet-synaptosomal Vmax coupling, results further suggest an important role of neuronal 5-HT reuptake in DMN regulation.

Indexed as

ConnectomeNeural PathwaysAdolescentAdultBlood PlateletsBrainFemaleFunctional NeuroimagingGenetic VariationHumansMagnetic Resonance ImagingMaleSerotoninSerotonin Plasma Membrane Transport ProteinsYoung AdultSerotoninSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, human

Identifiers

PMID24667541
PMCPMC3965432
OpenAlexW2067228275

What OpenQuestion 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 OpenQuestion graph.