Antidepressant imipramine diminishes stress-induced inflammation in the periphery and central nervous system and related anxiety- and depressive- like behaviors

Highlights • Imipramine ameliorated stress-induced inflammation in central nervous system. • Imipramine prevented stress- related anxiety- and depressive-like behaviors. • Imipramine attenuated stress-induced corticosterone and IL-6 responses in plasma. • Imipramine decreased the percentage of myelo...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2016-10, Vol.57, p.293-303
Main Authors: Ramirez, Karol, Sheridan, John F
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Antidepressive Agents, Tricyclic - administration & dosage
Antidepressive Agents, Tricyclic - pharmacology
Anxiety - etiology
Anxiety - immunology
Anxiety - metabolism
Anxiety - prevention & control
Anxiety-like behavior
Behavior, Animal
Corticosterone - blood
Depression - etiology
Depression - immunology
Depression - metabolism
Depression - prevention & control
Imipramine
Imipramine - administration & dosage
Imipramine - pharmacology
Inflammation - drug therapy
Inflammation - etiology
Inflammation - immunology
Inflammation - metabolism
Interleukin-6 - blood
Male
Mice
Mice, Inbred C57BL
Microglia
Myeloid Progenitor Cells - drug effects
Psychiatry
Psychosocial stress
Social avoidance
Social defeat
Spleen - drug effects
Spleen - immunology
Spleen - metabolism
Stress, Psychological - complications
Stress, Psychological - drug therapy
Stress, Psychological - immunology
Stress, Psychological - metabolism
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Summary:Highlights • Imipramine ameliorated stress-induced inflammation in central nervous system. • Imipramine prevented stress- related anxiety- and depressive-like behaviors. • Imipramine attenuated stress-induced corticosterone and IL-6 responses in plasma. • Imipramine decreased the percentage of myeloid progenitor cells in bone marrow, circulation, and brain. • Imipramine blocked neuroinflammatory signaling.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2016.05.008