Evidence map›Paper›PMID 24904293›Full record

ArticleFrontiers in cellular neuroscience2014

Distinctive behavioral and cellular responses to fluoxetine in the mouse model for Fragile X syndrome.

Marko Uutela, Jesse Lindholm, Tomi Rantamäki, Juzoh Umemori, Kerri Hunter, Vootele Võikar, Maija L Castrén

Abstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Review
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  3. Review
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  5. Review
  6. Article
  7. Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  8. Article
  9. Article
  10. Frontiers in molecular neuroscience · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Selective Disruption of Metabotropic Glutamate Receptor 5-Homer Interactions Mimics Phenotypes of Fragile X Syndrome in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  19. Review
  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

7 authors.

Marko UutelaInstitute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland.
Jesse LindholmNeuroscience Center, University of Helsinki Helsinki, Finland.
Tomi RantamäkiNeuroscience Center, University of Helsinki Helsinki, Finland.
Juzoh UmemoriNeuroscience Center, University of Helsinki Helsinki, Finland.
Kerri HunterInstitute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland.
Vootele VõikarNeuroscience Center, University of Helsinki Helsinki, Finland.
Maija L CastrénInstitute of Biomedicine/Physiology, University of Helsinki Helsinki, Finland ; Department of Child Neurology, Hospital for Children and Adolescents, University Hospital of Helsinki Helsinki, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fluoxetine is used as a therapeutic agent for autism spectrum disorder (ASD), including Fragile X syndrome (FXS). The treatment often associates with disruptive behaviors such as agitation and disinhibited behaviors in FXS. To identify mechanisms that increase the risk to poor treatment outcome, we investigated the behavioral and cellular effects of fluoxetine on adult Fmr1 knockout (KO) mice, a mouse model for FXS. We found that fluoxetine reduced anxiety-like behavior of both wild-type and Fmr1 KO mice seen as shortened latency to enter the center area in the open field test. In Fmr1 KO mice, fluoxetine normalized locomotor hyperactivity but abnormally increased exploratory activity. Reduced brain-derived neurotrophic factor (BDNF) and increased TrkB receptor expression levels in the hippocampus of Fmr1 KO mice associated with inappropriate coping responses under stressful condition and abolished antidepressant activity of fluoxetine. Fluoxetine response in the cell proliferation was also missing in the hippocampus of Fmr1 KO mice when compared with wild-type controls. The postnatal mRNA expression of serotonin transporter (SERT) was reduced in the thalamic nuclei of Fmr1 KO mice during the time of transient innervation of somatosensory neurons suggesting that developmental changes of SERT expression were involved in the differential cellular and behavioral responses to fluoxetine in wild-type and Fmr1 mice. The results indicate that changes of BDNF/TrkB signaling contribute to differential behavioral responses to fluoxetine among individuals with ASD.

Indexed as

autismBDNFbehaviorneurogenesisTrkB receptors

Identifiers

PMID24904293
PMCPMC4036306

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Registered trials

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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.