Evidence map›Paper›PMID 29141007›Full record

ArticlePloS one2017

Escitalopram and NHT normalized stress-induced anhedonia and molecular neuroadaptations in a mouse model of depression.

Or Burstein, Motty Franko, Eyal Gale, Assaf Handelsman, Segev Barak, Shai Motsan, Alon Shamir, Roni Toledano, Omri Simhon, Yafit Hirshler and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  18. Effects of Vitamin DNutrients · 2019
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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

12 authors at 5 institutions in 2 countries.

Or BursteinSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.
Motty FrankoSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.
Eyal GaleDepartment of Education and Psychology, The Open University, Raanana, Israel.
Assaf HandelsmanSchool of Psychological Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Segev BarakSchool of Psychological Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Shai MotsanSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.
Alon ShamirFaculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Roni ToledanoSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.
Omri SimhonSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.
Yafit HirshlerDepartment of Education and Psychology, The Open University, Raanana, Israel.
Gang ChenCenter for Translational Systems Biology and Neuroscience, Nanjing University of Chinese Medicine, Nanjing, China.
Ravid DoronSchool of Behavioral Science, The Academic College Tel-Aviv-Yaffo, Tel-Aviv, Israel.ORCID http://orcid.org/0000-0002-6523-9886
Academic College of Tel Aviv-Yafo · ILOpen University of Israel · ILTel Aviv University · ILNanjing University of Chinese Medicine · CNTechnion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anhedonia is defined as a diminished ability to obtain pleasure from otherwise positive stimuli. Anxiety and mood disorders have been previously associated with dysregulation of the reward system, with anhedonia as a core element of major depressive disorder (MDD). The aim of the present study was to investigate whether stress-induced anhedonia could be prevented by treatments with escitalopram or novel herbal treatment (NHT) in an animal model of depression. Unpredictable chronic mild stress (UCMS) was administered for 4 weeks on ICR outbred mice. Following stress exposure, animals were randomly assigned to pharmacological treatment groups (i.e., saline, escitalopram or NHT). Treatments were delivered for 3 weeks. Hedonic tone was examined via ethanol and sucrose preferences. Biological indices pertinent to MDD and anhedonia were assessed: namely, hippocampal brain-derived neurotrophic factor (BDNF) and striatal dopamine receptor D2 (Drd2) mRNA expression levels. The results indicate that the UCMS-induced reductions in ethanol or sucrose preferences were normalized by escitalopram or NHT. This implies a resemblance between sucrose and ethanol in their hedonic-eliciting property. On a neurobiological aspect, UCMS-induced reduction in hippocampal BDNF levels was normalized by escitalopram or NHT, while UCMS-induced reduction in striatal Drd2 mRNA levels was normalized solely by NHT. The results accentuate the association of stress and anhedonia, and pinpoint a distinct effect for NHT on striatal Drd2 expression.

Indexed as

AnhedoniaDisease Models, AnimalHerbal MedicineStress, PhysiologicalAnimalsAntidepressive Agents, Second-GenerationBrain-Derived Neurotrophic FactorCitalopramDepressionHippocampusMaleMiceMice, Inbred ICRReceptors, Dopamine D2RNA, MessengerAntidepressive Agents, Second-GenerationBrain-Derived Neurotrophic FactorCitalopramReceptors, Dopamine D2RNA, Messenger

Identifiers

PMID29141007
PMCPMC5687745
OpenAlexW2768846827

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.