Evidence map›Paper›PMID 17893702›Full record

ArticleMolecular psychiatry2008

Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin.

C Becker, B Zeau, C Rivat, A Blugeot, M Hamon, J-J Benoliel

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  14. Review
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  16. Novel Molecular Targets of Antidepressants.Molecules (Basel, Switzerland) · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Review

23 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

C BeckerFaculté de Médecine Pierre et Marie Curie, UMR 713 INSERM/UPMC, Douleurs et Stress, Paris Cedex, France. becker@ext.jussieu.fr
B Zeau
C Rivat
A Blugeot
M Hamon
J-J Benoliel
Sorbonne Université · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented. Here, we investigated whether CCKergic neurotransmission is relevant to depressive-like symptoms and antidepressant therapy using a novel preclinical model based on repeated social defeat over 4 weeks in rats. Repeated social defeat triggers changes that could be considered as behavioral and biological correlates of depressive symptoms in humans, such as a hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis (increase of serum corticosterone levels and of adrenal gland weight), increased immobility time in the forced swimming test (FST), decrease of body weight and of sweet water consumption and reduction of hippocampal volume associated with a decreased cell proliferation in the dentate gyrus. In addition, in vivo microdialysis showed that cortical CCK release was tonically increased in defeated rats. Chronic imipramine treatment (16 mg kg(-1) per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release. Chronic blockade of CCK2 receptors by the specific antagonist CI-988 (1 mg kg(-1) per day for 25 days) also normalized immobility time in the FST and prevented HPA axis hyperactivity, reduction of hippocampal volume and cell proliferation and decreased sweet water intake normally evoked by repeated social defeat. These data showed that the repeated social-defeat paradigm can be considered as a suitable model of 'depression' in rats. The causal link between social defeat-evoked (1) increase in cortical CCKergic neurotransmission and (2) depression-like symptoms that we highlighted here strongly suggests that CCKergic systems may be a relevant target for novel antidepressant therapy.

Indexed as

Dominance-SubordinationAnalysis of VarianceAnimalsAntidepressive Agents, TricyclicBromodeoxyuridineCell ProliferationCholecystokininCorticosteroneDepressionDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinHippocampusImipramineMaleMicrodialysisAntidepressive Agents, TricyclicBromodeoxyuridineCholecystokininCorticosteroneGlial Fibrillary Acidic ProteinImipraminePhosphopyruvate Hydratase

Identifiers

PMID17893702
OpenAlexW2075765747

What OpenQuestion holds

Textmetadata
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.