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Role of peripheral inflammation in central cytokine signaling, depression, and fear
Author(s) -
Tronson Natalie Celia,
Radulovic Jelena
Publication year - 2013
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.27.1_supplement.690.8
Subject(s) - cytokine , inflammation , medicine , depression (economics) , sickness behavior , prefrontal cortex , anxiety , population , myocardial infarction , immunology , hippocampus , psychology , psychiatry , cognition , environmental health , economics , macroeconomics
Activation of the innate immune system by chronic illness or injury is correlated with depression, anxiety and PTSD. In patients of heart attack (myocardial infarction, MI), rates of major depression and PTSD diagnoses are two‐ and three‐fold higher, respectively, than the population at large. Consistent with other patients, post‐MI incidence of PTSD and depression are correlated with increased levels of circulating pro‐ inflammatory cytokines. How circulating cytokines affect the brain remains unknown. We used a surgical model of myocardial infarction in mice to investigate the role of sustained peripheral inflammation on alterations in (1) fear conditioning and depression‐like behaviors (2) cytokine signaling in the brain and (3) sex differences in post‐ MI behavioral and inflammatory changes. Male, but not female mice exhibited enhanced fear conditioning soon after MI. Both males and females showed impaired memory and depression‐like behavior at later time points. 舲Within the hippocampus and prefrontal cortex, cytokine signaling and JAK/STAT3 were upregulated after MI in both female and male mice. The role of the cytokines and their downstream signaling in behavioral and emotional alterations are currently under investigation. These findings suggest cytokine‐dependent signaling as a candidate mechanism for susceptibility to, or development of depression and PTSD.