Oxytocin administration prevents cellular aging caused by social isolation.

Author: Stevenson JR1, McMahon EK2, Boner W3, Haussmann MF2
Author Information:
1Department of Psychology, Bucknell University, Lewisburg, PA, USA. Electronic address: j.stevenson@bucknell.edu.
2Department of Biology, Bucknell University, Lewisburg, PA, USA.
3Institute of Biodiversity Animal Health and Comparative Medicine, University of Glasgow, Scotland, United Kingdom.
Conference/Journal: Psychoneuroendocrinology.
Date published: 2019 Jan 8
Other: Volume ID: 103 , Pages: 52-60 , Special Notes: doi: 10.1016/j.psyneuen.2019.01.006. [Epub ahead of print] , Word Count: 182


Chronic stressors, such as chronic isolation in social mammals, can elevate glucocorticoids, which can affect cellular mechanisms of aging, including increased levels of oxidative stress and shortened telomere lengths. Recent work in the selectively social prairie vole (Microtus ochrogaster) suggests that oxytocin and social support may mitigate some of the negative consequences of social isolation, possibly by reducing glucocorticoid levels. We investigated the influences of isolation, social support, and daily oxytocin injections in female prairie voles. Glucocorticoid levels, oxidative damage, telomere length, and anhedonia, a behavioral index of depression, were measured throughout the study. We found that six weeks of chronic isolation led to increased glucocorticoid levels, oxidative damage, telomere degradation and anhedonia. However, daily oxytocin injections in isolated voles prevented these negative consequences. These findings demonstrate that chronic social isolation in female prairie voles is a potent stressor that results in depression-like behavior and accelerated cellular aging. Importantly, oxytocin can completely prevent the negative consequences of social isolation.

Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.

KEYWORDS: Aging; Oxidative stress; Oxytocin; Social support; Stress; Telomeres

PMID: 30640038 DOI: 10.1016/j.psyneuen.2019.01.006

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