There is a bidirectional association between depression and cardiovascular disease. The neurobiological mechanisms underlying this association may involve an inability to cope with disrupted social bonds. This study investigated in an animal model the integration of depressive behaviors and cardiac dysfunction after a disrupted social bond and during an operational measure of depression, relative to the protective effects of intact social bonds.
Depressive behaviors in the forced swim test and continuous electrocardiographic parameters were measured in 14 adult, female socially monogamous prairie voles (rodents), after 4 weeks of social pairing or isolation.
After social isolation, animals exhibited (all values are mean ± standard error of the mean; isolated versus paired, respectively) increased heart rate (416 ± 14 versus 370 ± 14 bpm, p < .05) and reduced heart rate variability (3.3 ± 0.2 versus 3.9 ± 0.2 ln(ms2)). During the forced swim test, isolated animals exhibited greater helpless behavior (immobility = 106 ± 11 versus 63 ± 11 seconds, p < .05), increased heart rate (530 ± 22 versus 447 ± 15 bpm, p < .05), reduced heart rate variability (1.8 ± 0.4 versus 2.7 ± 0.2 ln(ms2), p < .05), and increased arrhythmias (arrhythmic burden score = 181 ± 46 versus 28 ± 12, p < .05).
The display of depressive behaviors during an operational measure of depression is coupled with increased heart rate, reduced heart rate variability, and increased arrhythmias, indicative of dysfunctional behavioral and physiological stress coping abilities as a function of social isolation. In contrast, social pairing with a sibling is behaviorally protective and cardioprotective. The present results can provide insight into a possible social mechanism underlying the association between depression and cardiovascular disease in humans.
ANOVA = analysis of variance
DSI = Data Sciences International
ECG = electrocardiographic
FST = forced swim test
HR = heart rate
RSA = respiratory sinus arrhythmia
SDNN = standard deviation of normal-to-normal intervals
SEM = standard error of the mean
From the Department of Psychology (A.J.G., S.L.B., D.L.C., N.M., K.P.), Northern Illinois University, DeKalb, Illinois; Department of Physiology and Pharmacology (J.A.M., A.J.J.), Des Moines University, Des Moines, Iowa; and Stress Physiology Lab (A.S.), Department of Evolutionary and Functional Biology, University of Parma, Parma, Italy.
Address correspondence and reprint requests to Angela J. Grippo, PhD, Department of Psychology, Northern Illinois University, PM 357, DeKalb, IL 60115. E-mail: firstname.lastname@example.org
This research was supported by the National Institutes of Health (Grants MH73233 and MH77581).
Received for publication November 10, 2011; revision received January 27, 2012.