To investigate the hypothesis that long-term social isolation in an animal model would produce depression-relevant behaviors and disruptions in the 24-hour autonomic and activity parameters, and to further demonstrate the utility and validity of an animal model for the study of social environment, behavior, and autonomic function. Converging evidence from both experimental and epidemiological studies indicates that there is a bidirectional association between depression and cardiovascular disease; however, the precise neurobiological mechanisms underlying this relationship are not well understood. Disruptions in the social environment may influence this relationship.
Depression-relevant behaviors and ambulatory electrocardiographic and activity data were measured in 12 adult, socially monogamous prairie voles (rodents) during a period of chronic social isolation or social pairing (control conditions).
Prairie voles exposed to 4 weeks of social isolation versus control conditions (social pairing) exhibited anhedonia, increased 24-hour heart rate, reduced 24-hour heart rate variability, and predictable correlations between the behavioral measure (anhedonia) and the autonomic measures.
Social isolation is associated with depressive behaviors, 24-hour autonomic dysfunction, and predictable interrelationships between these variables in prairie voles but does not seem to be associated with rhythmicity changes in activity level or autonomic function. These findings have implications for understanding the role of the social environment in mediating the association of mood and cardiovascular disorders in humans.
ANOVA = analysis of variance; DSI = Data Sciences International; ECG = electrocardiographic; HR = heart rate; RSA = respiratory sinus arrhythmia; SDNN = standard deviation of normal-to-normal intervals.
From the Department of Psychology (A.J.G., N.M., D.L.C., M.A.L., S.L.B.), Northern Illinois University, DeKalb, Illinois; and the Department of Psychiatry and Brain-Body Center (C.S.C., S.W.P.), University of Illinois at Chicago, Chicago, Illinois.
Address correspondence and reprint requests to Angela J. Grippo, PhD, Department of Psychology, Northern Illinois University, PM 357, DeKalb, IL 60115. E-mail: email@example.com
Received for publication April 15, 2010; revision received September 2, 2010.
This research was supported, in part, by Grants MH72935 (C.S.C.), MH73233 (A.J.G.), MH77581 (A.J.G.), and MH67446 (S.W.P.) from the National Institutes of Health.