1. Neuroscience
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A reduction in voluntary physical activity in early pregnancy in mice is mediated by prolactin

  1. Sharon R Ladyman  Is a corresponding author
  2. Kirsten M Carter
  3. Matt L Gillett
  4. Zin Khant Aung
  5. David R Grattan  Is a corresponding author
  1. University of Otago, New Zealand
Research Article
  • Cited 2
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Cite this article as: eLife 2021;10:e62260 doi: 10.7554/eLife.62260

Abstract

As part of the maternal adaptations to pregnancy, mice show a rapid, profound reduction in voluntary running wheel activity (RWA) as soon as pregnancy is achieved. Here, we evaluate the hypothesis that prolactin, one of the first hormones to change secretion pattern following mating, is involved in driving this suppression of physical activity levels during pregnancy. We show that prolactin can acutely suppress RWA in non-pregnant female mice, and that conditional deletion of prolactin receptors (Prlr) from either most forebrain neurons or from GABA neurons prevented the early pregnancy-induced suppression of RWA. Deletion of Prlr specifically from the medial preoptic area, a brain region associated with multiple homeostatic and behavioural roles including parental behaviour, completely abolished the early pregnancy-induced suppression of RWA. As pregnancy progresses, prolactin action continues to contribute to the further suppression of RWA, although it is not the only factor involved. Our data demonstrate a key role for prolactin in suppressing voluntary physical activity during early pregnancy, highlighting a novel biological basis for reduced physical activity in pregnancy.

Data availability

All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for Figures 4-6.

Article and author information

Author details

  1. Sharon R Ladyman

    Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand
    For correspondence
    sharon.ladyman@otago.ac.nz
    Competing interests
    The authors declare that no competing interests exist.
  2. Kirsten M Carter

    Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand
    Competing interests
    The authors declare that no competing interests exist.
  3. Matt L Gillett

    Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand
    Competing interests
    The authors declare that no competing interests exist.
  4. Zin Khant Aung

    Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-5121-2770
  5. David R Grattan

    Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand
    For correspondence
    dave.grattan@otago.ac.nz
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-5606-2559

Funding

Health Research Council of New Zealand (14-568)

  • David R Grattan

University of Otago

  • Sharon R Ladyman

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Animal experimentation: This study was performed in strict accordance with the Animal Welfare Act (1999) New Zealand. All experimental protocols were approved by the University of Otago Animal Ethics Committee (Animal Use Protocol 36-17).

Reviewing Editor

  1. Margaret M McCarthy, University of Maryland School of Medicine, United States

Publication history

  1. Received: August 19, 2020
  2. Preprint posted: September 11, 2020 (view preprint)
  3. Accepted: September 13, 2021
  4. Accepted Manuscript published: September 16, 2021 (version 1)
  5. Version of Record published: September 29, 2021 (version 2)

Copyright

© 2021, Ladyman et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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