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Individual differences in susceptibility to depression and cardiovascular disease comorbidity in a rat model of social stress (1074.10)
Author(s) -
Lombard Calliandra,
Melson Michael,
Wood Susan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1074.10
Subject(s) - anhedonia , comorbidity , medicine , coping (psychology) , disease , phenotype , psychosocial , social defeat , social stress , psychology , clinical psychology , endocrinology , psychiatry , biology , genetics , gene , dopamine
Psychosocial stress precipitates psychiatric disorders (eg, depression) and cardiovascular disease in vulnerable individuals, but underlying mechanisms remain unknown. We previously identified two distinct phenotypic responses to social stress in rats (resident‐intruder model), characterized by either passive coping, assuming defeat within a short latency (SL, 343±7) or by proactive coping behaviors and longer defeat latencies (LL, 571±53). The SL phenotype was associated with endocrine and behavioral characteristics resembling depression and decreased heart rate variability indicating greater cardiovascular disease risk. The present study characterized the impact of stress coping on susceptibility to a depressive‐like phenotype with comorbid hypertension in rats exposed to 7 (30 min/day) social defeat or control manipulations. 24‐hr ECG and pressure telemetry revealed persistent elevations in resting mean arterial pressure (MAP) selectively in the SL phenotype as early as the 4th day (change from day 0: con 0.4 ± 2, SL 7.1 ± 2, LL 2.5 ± 0.9). Interestingly, sucrose intake measured 7 days post stress was negatively correlated with changes in MAP (r= ‐0.34, p=0.03), indicating an association between anhedonia and increased MAP. These studies also sought to determine the impact of these cardiovascular changes on susceptibility to isoproterenol‐induced arrhythmias. These data suggest passive stress coping promotes vulnerability to a depressive‐cardiovascular disease‐like phenotype, while active coping confers resilience. Future studies will utilize this model to identify critical brain regions underlying the pathogenesis of depression‐cardiovascular disease comorbidity. Grant Funding Source : Supported by NARSAD 17830 and 13BGIA 14370026 to SKW