Evidence map›Paper›PMID 26363094›Full record

ArticleBrain research2015

Hyperactivity and depression-like traits in Bax KO mice.

Thomas E Krahe, Alexandre E Medina, Crystal L Lantz, Cláudio C Filgueiras

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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  5. Review
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

4 authors at 4 institutions in 2 countries.

Thomas E KraheDepartamento de Ciências Fisiológicas, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil; Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, USA.
Alexandre E MedinaDepartment of Pediatrics, University of Maryland, Baltimore, USA.
Crystal L LantzDepartment of Biology, University of Maryland, College Park, USA.
Cláudio C FilgueirasDepartamento de Ciências Fisiológicas, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: ccfilg@pq.cnpq.br.
Universidade do Estado do Rio de Janeiro · BRUniversity of Maryland, Baltimore · USUniversity of Maryland, College Park · USVirginia Commonwealth University Medical Center · US

Funding

Amplifier Replacement for Slice Electrophysiology StudiesR01AA013023 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI MEDINA, ALEXANDRE ESTEVES · 2001 to 2021
$6.3M
Improving Neuronal Plasticity in a Mouse Model of FASDR01AA022455 · NIAAA · UNIVERSITY OF MARYLAND BALTIMORE · PI MEDINA, ALEXANDRE ESTEVES · 2014 to 2018
$1.6M
NIAAA NIH HHS R01 AA013023NIAAA NIH HHS R01 AA022455NIAAA NIH HHS R01AA13023
6 · The paper itself

Abstract

The Bax gene is a member of the Bcl-2 gene family and its pro-apoptotic Bcl-associated X (Bax) protein is believed to be crucial in regulating apoptosis during neuronal development as well as following injury. With the advent of mouse genomics, mice lacking the pro-apoptotic Bax gene (Bax KO) have been extensively used to study how cell death helps to determine synaptic circuitry formation during neurodevelopment and disease. Surprisingly, in spite of its wide use and the association of programmed neuronal death with motor dysfunctions and depression, the effects of Bax deletion on mice spontaneous locomotor activity and depression-like traits are unknown. Here we examine the behavioral characteristics of Bax KO male mice using classical paradigms to evaluate spontaneous locomotor activity and depressive-like responses. In the open field, Bax KO animals exhibited greater locomotor activity than their control littermates. In the forced swimming test, Bax KO mice displayed greater immobility times, a behavior despair state, when compared to controls. Collectively, our findings corroborate the notion that a fine balance between cell survival and death early during development is critical for normal brain function later in life. Furthermore, it points out the importance of considering depressive-like and hyperactivity behavioral phenotypes when conducting neurodevelopmental and other studies using the Bax KO strain.

Indexed as

Analysis of VarianceAnimalsbcl-2-Associated X ProteinCell SurvivalDepressionDisease Models, AnimalExploratory BehaviorHyperkinesisMaleMiceMice, Inbred C57BLMice, KnockoutSwimmingTime FactorsBax protein, mousebcl-2-Associated X ProteinApoptosisBcl-2 protein familyBehavioral phenotypingBehavior despairDepressive-like behaviorLocomotor hyperactivityNeuronal cell death

Identifiers

PMID26363094
PMCPMC5806998
OpenAlexW1411241211

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.