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Individual differences in vulnerability to social stress‐induced cardiac dysfunction in rats
Author(s) -
Wood Susan K,
McFadden Kile V,
Bhatnagar Seema,
Valentino Rita J
Publication year - 2010
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.24.1_supplement.768.3
Subject(s) - social defeat , locus coeruleus , stimulation , medicine , endocrinology , hypothalamus , amygdala , behavioural despair test , psychology , social stress , population , neuroscience , central nervous system , hippocampus , environmental health , antidepressant
Social stress precipitates cardiovascular disorders that are likely mediated by exaggerated noradrenergic stimulation. Differing coping strategies result in varying levels of noradrenergic stimulation and may underlie susceptibility to stress‐induced cardiovascular alterations. Repeated social defeat (7 days) using a rat resident‐intruder model resulted in the emergence of two phenotypes. One population (~45%) exhibited a passive response (e.g., freezing) and assumed a defeat posture within a short latency (SL; 197±15s). The other phenotype (~55%) exhibited proactive behaviors (e.g., upright posture) and a longer defeat latency (LL; 438±12s). In vivo telemetry on days 1, 4, and 7 of defeat revealed that LL rats exhibited greater heart rate at rest and during defeat than SL, and resulted in greater cardiac weight. Neuronal activation (cFos) of noradrenergic neurons within the locus coeruleus and dorsal motor vagus was greater in LL rats, while areas mediating the neuroendocrine stress response (paraventricular nucleus, hypothalamus) and freezing behaviors (medial amygdala) were greater in SL rats. SL rats also exhibited more depressive‐like behaviors in the forced swim test. These data suggest that passively coping with social stress renders vulnerability to psychological disorder whereas active coping increases susceptibility to cardiovascular dysfunction. MH 40008, AHA 0825572D, MH06751 to SB