Evidence map›Paper›PMID 21679928›Full record

ArticleBiological psychiatry2011

FosB is essential for the enhancement of stress tolerance and antagonizes locomotor sensitization by ΔFosB.

Yoshinori N Ohnishi, Yoko H Ohnishi, Masaaki Hokama, Hiroko Nomaru, Katsuhisa Yamazaki, Yohei Tominaga, Kunihiko Sakumi, Eric J Nestler, Yusaku Nakabeppu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Biological psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Fluoxetine epigenetically alters the CaMKIIα promoter in nucleus accumbens to regulate ΔFosB binding and antidepressant effects.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
    Article
  15. Article
  16. Review
  17. fosB-null mice display impaired adult hippocampal neurogenesis and spontaneous epilepsy with depressive behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Article
  18. Article
  19. Article
  20. Review of pharmacological treatment in mood disorders and future directions for drug development.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Yoshinori N OhnishiDivision of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, USA.
Yoko H Ohnishi
Masaaki Hokama
Hiroko Nomaru
Katsuhisa Yamazaki
Yohei Tominaga
Kunihiko Sakumi
Eric J Nestler
Yusaku Nakabeppu
Kyushu University · JPIcahn School of Medicine at Mount Sinai · US

Funding

Using neuroeconomics to disentangle the transcriptional mechanisms underlying resilience versus susceptibility to stressR01MH051399 · NIMH · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1994 to 2023
$10.2M
MOLECULAR STUDIES OF COCAINE ACTION IN BRAINR37DA007359 · NIDA · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1996 to 2020
$6.9M
Molecular Studies of Cocaine Action in BrainR01DA007359 · NIDA · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1991 to 2025
$5.6M
NIDA NIH HHS R01 DA007359NIDA NIH HHS R37 DA007359NIMH NIH HHS R01 MH051399
6 · The paper itself

Abstract

backgroundMolecular mechanisms underlying stress tolerance and vulnerability are incompletely understood. The fosB gene is an attractive candidate for regulating stress responses, because ΔFosB, an alternative splice product of the fosB gene, accumulates after repeated stress or antidepressant treatments. On the other hand, FosB, the other alternative splice product of the fosB gene, expresses more transiently than ΔFosB but exerts higher transcriptional activity. However, the functional differences of these two fosB products remain unclear.

methodsWe established various mouse lines carrying three different types of fosB allele, wild-type (fosB(+)), fosB-null (fosB(G)), and fosB(d) allele, which encodes ΔFosB but not FosB, and analyzed them in stress-related behavioral tests.

resultsBecause fosB(+/d) mice show enhanced ΔFosB levels in the presence of FosB and fosB(d/d) mice show more enhanced ΔFosB levels in the absence of FosB, the function of FosB can be inferred from differences observed between these lines. The fosB(+/d) and fosB(d/d) mice showed increased locomotor activity and elevated Akt phosphorylation, whereas only fosB(+/d) mice showed antidepressive-like behaviors and increased E-cadherin expression in striatum compared with wild-type mice. In contrast, fosB-null mice showed increased depression-like behavior and lower E-cadherin expression.

conclusionsThese findings indicate that FosB is essential for stress tolerance mediated by ΔFosB. These data suggest that fosB gene products have a potential to regulate mood disorder-related behaviors.

Indexed as

Adaptation, PsychologicalAnimalsCadherinsCorpus StriatumDopamineExploratory BehaviorMaleMaze LearningMiceMice, Mutant StrainsMotor ActivityProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fosStress, PsychologicalCadherinsDopamineFosb protein, mouseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fos

Identifiers

PMID21679928
PMCPMC3264950
OpenAlexW1978715650

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.