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Amylin-Calcitonin receptor signaling in the medial preoptic area mediates affiliative social behaviors in female mice

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  • Kansai Fukumitsu

    (RIKEN Center for Brain Science)

  • Misato Kaneko

    (RIKEN Center for Brain Science
    Nippon Veterinary and Life Science University, Musashino)

  • Teppo Maruyama

    (RIKEN Center for Brain Science
    Nippon Veterinary and Life Science University, Musashino)

  • Chihiro Yoshihara

    (RIKEN Center for Brain Science)

  • Arthur J. Huang

    (RIKEN Center for Brain Science)

  • Thomas J. McHugh

    (RIKEN Center for Brain Science)

  • Shigeyoshi Itohara

    (RIKEN Center for Brain Science)

  • Minoru Tanaka

    (Nippon Veterinary and Life Science University, Musashino)

  • Kumi O. Kuroda

    (RIKEN Center for Brain Science)

Abstract

Social animals actively engage in contact with conspecifics and experience stress upon isolation. However, the neural mechanisms coordinating the sensing and seeking of social contacts are unclear. Here we report that amylin-calcitonin receptor (Calcr) signaling in the medial preoptic area (MPOA) mediates affiliative social contacts among adult female mice. Isolation of females from free social interactions first induces active contact-seeking, then depressive-like behavior, concurrent with a loss of Amylin mRNA expression in the MPOA. Reunion with peers induces physical contacts, activates both amylin- and Calcr-expressing neurons, and leads to a recovery of Amylin mRNA expression. Chemogenetic activation of amylin neurons increases and molecular knockdown of either amylin or Calcr attenuates contact-seeking behavior, respectively. Our data provide evidence in support of a previously postulated origin of social affiliation in mammals.

Suggested Citation

  • Kansai Fukumitsu & Misato Kaneko & Teppo Maruyama & Chihiro Yoshihara & Arthur J. Huang & Thomas J. McHugh & Shigeyoshi Itohara & Minoru Tanaka & Kumi O. Kuroda, 2022. "Amylin-Calcitonin receptor signaling in the medial preoptic area mediates affiliative social behaviors in female mice," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-28131-z
    DOI: 10.1038/s41467-022-28131-z
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    References listed on IDEAS

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