Evidence map›Paper›PMID 26747511›Full record

ArticleMolecular brain2016

Activation of protein kinase A in the amygdala modulates anxiety-like behaviors in social defeat exposed mice.

Liu Yang, Li-Jun Shi, Jin Yu, Yu-Qiu Zhang

Abstract read
In one paragraph

Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
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  4. Review
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  11. Social modulation of ageing: mechanisms, ecology, evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Empathy for Distress in Humans and Rodents.Neuroscience bulletin · 2018
    Review
  16. Article
  17. Article
  18. Article
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  20. Article
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.

Liu YangInstitute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, 1202 Mingdao Building, 131 Dong An Road, Shanghai, 200032, China. ribaike@163.com.
Li-Jun ShiInstitute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, 1202 Mingdao Building, 131 Dong An Road, Shanghai, 200032, China. benben231016@163.com.
Jin YuDepartment of Integrative Medicine and Neurobiology, Shanghai Medical School, Fudan University, Shanghai, 200032, China. yujin@shmu.edu.cn.
Yu-Qiu ZhangInstitute of Neurobiology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, 1202 Mingdao Building, 131 Dong An Road, Shanghai, 200032, China. yuqiuzhang@fudan.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSocial defeat (SD) stress induces social avoidance and anxiety-like phenotypes. Amygdala is recognized as an emotion-related brain region such as fear, aversion and anxiety. It is conceivable to hypothesize that activation of amygdala is involved in SD-dependent behavioral defects.

resultsSD model was established using C57BL/6J mice that were physically defeated by different CD-1 mice for 10 days. Stressed mice exhibited decreased social interaction level in social interaction test and significant anxiety-like behaviors in elevated plus maze and open field tests. Meanwhile, a higher phosphorylation of PKA and CREB with a mutually linear correlation, and increased Fos labeled cells in the basolateral amygdala (BLA) were observed. Activation of PKA in the BLA by 8-Br-cAMP, a PKA activitor, significantly upregulated pCREB and Fos expression. To address the role of PKA activation on SD stress-induced social avoidance and anxiety-like behaviors, 8-Br-cAMP or H-89, a PKA inhibitor, was continuously administered into the bilateral BLA by a micro-osmotic pump system during the 10-day SD period. Neither H-89 nor 8-Br-cAMP affected the social behavior. Differently, 8-Br-cAMP significantly relieved anxiety-like behaviors in both general and moderate SD protocols. H-89 per se did not have anxiogenic effect in naïve mice, but aggravated moderate SD stress-induced anxiety-like behaviors. The antidepressant clomipramine reduced SD-induced anxiety and up-regulated pPKA level in the BLA.

conclusionsThese results suggest that SD-driven PKA activation in the basolateral amygdala is actually a compensatory rather than pathogenic response in the homeostasis, and modulating amygdaloid PKA may exhibit potency in the therapy of social derived disorders.

Indexed as

Social BehaviorAmygdalaAnimalsAnxietyAvoidance LearningClomipramineCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEnzyme ActivationMaleMice, Inbred C57BLPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-fosSignal TransductionStress, PsychologicalClomipramineCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinProtein Kinase InhibitorsProto-Oncogene Proteins c-fos

Identifiers

PMID26747511
PMCPMC4706664

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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.