Evidence map›Paper›PMID 25522426›Full record

ArticleThe international journal of neuropsychopharmacology2014

Diurnal oscillation of amygdala clock gene expression and loss of synchrony in a mouse model of depression.

Giorgia Savalli, Weifei Diao, Stefan Schulz, Kristina Todtova, Daniela D Pollak

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Intestinal Clock Promotes Cognitive Memory Through Adenosine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  12. Circadian rhythm and atherosclerosis (Review).Experimental and therapeutic medicine · 2020
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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

5 authors at 1 institution in 1 country.

Giorgia SavalliDepartment of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
Weifei DiaoDepartment of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
Stefan SchulzDepartment of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
Kristina TodtovaDepartment of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
Daniela D PollakDepartment of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria. daniela.pollak@meduniwien.ac.at.
Medical University of Vienna · AT

Funding

Austrian Science Fund FWF P 22424
6 · The paper itself

Abstract

backgroundDisturbances in circadian rhythm-related physiological and behavioral processes are frequently observed in depressed patients and several clock genes have been identified as risk factors for the development of mood disorders. However, the particular involvement of the circadian system in the pathophysiology of depression and its molecular regulatory interface is incompletely understood.

methodsA naturalistic animal model of depression based upon exposure to chronic mild stress was used to induce anhedonic behavior in mice. Micro-punch dissection was used to isolate basolateral amygdala tissue from anhedonic mice followed by quantitative real-time PCR-based analysis of gene expression.

resultsHere we demonstrate that chronic mild stress-induced anhedonic behavior is associated with disturbed diurnal oscillation of the expression of Clock, Cry2, Per1, Per3, Id2, Rev-erbα, Ror-β and Ror-γ in the mouse basolateral amygdala. Clock gene desynchronization was accompanied by disruption of the diurnal expressional pattern of vascular endothelial growth factor A expression in the basolateral amygdala of anhedonic mice, also reflected in alterations of circulating vascular endothelial growth factor A levels.

conclusionWe propose that aberrant control of diurnal rhythmicity related to depression may indeed directly result from the illness itself and establish an animal model for the further exploration of the molecular mechanisms mediating the involvement of the circadian system in the pathophysiology of mood disorders.

Indexed as

AnhedoniaCircadian RhythmAmygdalaAnimalsBehavior, AnimalCLOCK ProteinsDepressionGene ExpressionMaleMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionStress, PsychologicalCLOCK Proteinsamygdalachronic mild stressclock genedepressionVEGF

Identifiers

PMID25522426
PMCPMC4376549
OpenAlexW2055730682

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.