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Leptin enhances social motivation and reverses chronic unpredictable stress-induced social anhedonia during adolescence

*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Research
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Social anhedonia, a loss of interest and pleasure in social interactions, is a common symptom of major depression as well as other psychiatric disorders. Depression can occur at any age, but typically emerges in adolescence or early adulthood, which represents a sensitive period for social interaction that is vulnerable to stress. In this study, we evaluated social interaction reward using a conditioned place preference (CPP) paradigm in adolescent male and female mice. Adolescent mice of both sexes exhibited a preference for the social interaction-associated context. Chronic unpredictable stress (CUS) impaired the development of CPP for social interaction, mimicking social anhedonia in depressed adolescents. Conversely, administration of leptin, an adipocyte-derived hormone, enhanced social interaction-induced CPP in non-stressed control mice and reversed social anhedonia in CUS mice. By dissecting the motivational processes of social CPP into social approach and isolation avoidance components, we demonstrated that leptin treatment increased isolation aversion without overt social reward effect. Further mechanistic exploration revealed that leptin stimulated oxytocin gene transcription in the paraventricular nucleus of the hypothalamus, while oxytocin receptor blockade abolished the leptin-induced enhancement of socially-induced CPP. These results establish that chronic unpredictable stress can be used to study social anhedonia in adolescent mice and provide evidence that leptin modulates social motivation possibly via increasing oxytocin synthesis and oxytocin receptor activation.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Research
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 4948-4958 (11 pages)

Journal (Volume, Issue Number)

Molecular Psychiatry (Volume 27, Issue 12)

Publication milestones

  • Accepted/In press - 2022
  • Published - 12/2022

Publication status

Published - 12/2022

ISSN

1359-4184

Publication IDs

  • Scopus: 85138505560
  • PubMed: 36138127

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0.57
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3
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1
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Funding Details

This work was supported by NSFC81771458 (to MG) and NIH grants MH100583, MH119456 and AG062166 (to XYL), and AG064895 (to XYL and NLW).
FundersFunding numbers
NSFC81771458
-
NIH
MH119456, AG062166, MH100583, AG064895
NHLBI
R01HL142097