Evidence map›Paper›PMID 22113448›Full record

ArticlePsychopharmacology2012

Evaluating genetic markers and neurobiochemical analytes for fluoxetine response using a panel of mouse inbred strains.

Cristina S Benton, Brooke H Miller, Sean Skwerer, Oscar Suzuki, Laura E Schultz, Michael D Cameron, J S Marron, Mathew T Pletcher, Tim Wiltshire

Open access · hybridAbstract read
In one paragraph

Article in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 32% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Apolipoprotein D as a Potential Biomarker in Neuropsychiatric Disorders.International journal of molecular sciences · 2023
    Review
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  13. Slow-release delivery enhances the pharmacological properties of oral 5-hydroxytryptophan: mouse proof-of-concept.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
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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

9 authors at 3 institutions in 1 country.

Cristina S BentonDivision of Pharmacotherapy and Experimental Therapeutics, University of North Carolina at Chapel Hill, Genetic Medicine Building, 120 Mason Farm Road, Chapel Hill, NC 27599, USA.
Brooke H Miller
Sean Skwerer
Oscar Suzuki
Laura E Schultz
Michael D Cameron
J S Marron
Mathew T Pletcher
Tim Wiltshire
University of North Carolina at Chapel Hill · USScripps Research Institute · USPfizer (United States) · US

Funding

Organismal, Cellular, and Genetic Networks in Anxiety and DepressionR01MH077251 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILTSHIRE, TIM · 2007 to 2012
$1.7M
Genetic regulation of basal and antidepressant-induced adult neurogenesisF32MH084528 · NIMH · SCRIPPS FLORIDA · PI MILLER, BROOKE H · 2008 to 2010
$148k
NIMH NIH HHS 1R01MH077251NIMH NIH HHS F32 MH084528NIMH NIH HHS F32MH084528NIMH NIH HHS R01 MH077251
6 · The paper itself

Abstract

rationaleIdentification of biomarkers that establish diagnosis or treatment response is critical to the advancement of research and management of patients with depression.

objectiveOur goal was to identify biomarkers that can potentially assess fluoxetine response and risk to poor treatment outcome.

methodsWe measured behavior, gene expression, and the levels of 36 neurobiochemical analytes across a panel of genetically diverse mouse inbred lines after chronic treatment with water or fluoxetine.

resultsGlyoxylase 1 (GLO1) and guanine nucleotide-binding protein 1 (GNB1) mostly account for baseline anxiety-like and depressive-like behavior, indicating a common biological link between depression and anxiety. Fluoxetine-induced biochemical alterations discriminated positive responders, while baseline neurobiochemical differences differentiated negative responders (p < 0.006). Results show that glial fibrillary acidic protein, S100 beta protein, GLO1, and histone deacetylase 5 contributed most to fluoxetine response. These proteins are linked within a cellular growth/proliferation pathway, suggesting the involvement of cellular genesis in fluoxetine response. Furthermore, a candidate genetic locus that associates with baseline depressive-like behavior contains a gene that encodes for cellular proliferation/adhesion molecule (Cadm1), supporting a genetic basis for the role of neuro/gliogenesis in depression.

conclusionWe provided a comprehensive analysis of behavioral, neurobiochemical, and transcriptome data across 30 mouse inbred strains that has not been accomplished before. We identified biomarkers that influence fluoxetine response, which, altogether, implicate the importance of cellular genesis in fluoxetine treatment. More broadly, this approach can be used to assess a wide range of drug response phenotypes that are challenging to address in human samples.

Indexed as

AnimalsBehavior, AnimalFluoxetineGene Expression ProfilingGene Expression RegulationGenetic MarkersMaleMiceMice, Inbred StrainsSelective Serotonin Reuptake InhibitorsFluoxetineGenetic MarkersSelective Serotonin Reuptake Inhibitors

Identifiers

PMID22113448
PMCPMC3337404
OpenAlexW2024542458

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.