322
Views
7
CrossRef citations to date
0
Altmetric
Original Articles

Behavioral and cardiovascular consequences of disrupted oxytocin communication in cohabitating pairs of male and female prairie voles

, , ORCID Icon, , &
Pages 649-662 | Received 24 Sep 2018, Accepted 07 Jan 2019, Published online: 31 Jan 2019
 

ABSTRACT

Negative social experiences may influence psychological and physiological health via altered central oxytocin communication. The prairie vole is valuable for investigating the potential influence of oxytocin on responses to social experiences. Prairie voles are socially monogamous, live in pairs or family groups, and respond negatively to changes in the social environment. This study investigated the hypothesis that disruptions of oxytocin in one prairie vole of a cohabitating male-female pair would alter social behavior in that specific animal; and these behavioral changes in turn would influence the untreated partner’s behavior and physiology. Pharmacological antagonism of oxytocin with the receptor antagonist L-368,899 in the male prairie vole disrupted social behaviors between the male and his untreated female partner. This manipulation also negatively influenced the behavior and cardiovascular function in the untreated female partner, including increased: (a) depression-relevant behaviors in two behavioral stressors, (b) basal mean arterial pressure and heart rate, and (c) cardiovascular reactivity to the behavioral stressors. These results suggest that disruptions of oxytocin and social behavior in one animal may produce indicators of social stress in an untreated social partner. This preliminary research provides a foundation for future studies to investigate mechanisms underlying responses to social experiences in humans.

Acknowledgments

This article is dedicated to Professor John T. Cacioppo – colleague, dear friend, and husband – whose innovative ideas and unwavering work ethic continually motivated us to try harder. Thank you to Merck Sharpe and Dohme Corp. (Rahway, NJ) for the generous donation of L-368,899 through a Material Transfer Agreement. Thank you also to William Colburn, Miranda Cox, Elliott Ihm, Marigny Normann, Amir Toghraee, and Matthew Woodbury for valuable assistance.

Disclosure statement

No potential conflict of interest was reported by the authors.

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

Preparation of this manuscript was supported in part by Grant No. [R15HL112350] from the National Heart, Lung and Blood Institute awarded to AJG, Grant No. [R01AG033590] from the National Institute on Aging awarded to SC, and the donation of L-368,899 from Merck Sharpe and Dohme Corp. awarded to AJG. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.