Format

Send to

Choose Destination
See comment in PubMed Commons below
Auton Neurosci. 2010 Aug 25;156(1-2):44-50. doi: 10.1016/j.autneu.2010.03.003. Epub 2010 Mar 27.

Cardiac dysfunction and hypothalamic activation during a social crowding stressor in prairie voles.

Author information

1
Department of Psychology, Northern Illinois University, DeKalb, IL, USA. angelagrippo@niu.edu

Abstract

Negative social interactions produce several detrimental consequences in humans and non-human animals; and conversely, positive social interactions may have stress-buffering effects on both behavior and physiology. However, the mechanisms underlying specific stressor-responsiveness in the context of the social environment are not well understood. The present study investigated the integration of behavior, cardiac function, and Fos-immunoreactivity in the hypothalamic paraventricular nucleus during an acute social stressor in female, socially monogamous prairie voles exposed to previous long-term pairing (control conditions) or isolation. Animals previously exposed to social isolation displayed increased heart rate, attenuated heart rate variability, and increased incidence of cardiac arrhythmias during an acute crowding stressor versus animals previously exposed to social pairing; these cardiac alterations were not secondary to behavioral changes during the crowding stressor. Furthermore, social isolation was associated with increased c-Fos-immunoreactivity in the hypothalamic paraventricular nucleus following the crowding stressor, versus social pairing. The prairie vole provides a useful model for understanding how the social environment contributes to changes in behavior, cardiac function, and central stress-regulatory processes in humans.

PMID:
20347401
PMCID:
PMC2914185
DOI:
10.1016/j.autneu.2010.03.003
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center