Dynamic cross-talk between microglia and peripheral monocytes underlies stress-induced neuroinflammation and behavioral consequences.
Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2017-10-01; 79: 40-48
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1. Prog Neuropsychopharmacol Biol Psychiatry. 2017 Oct 3;79(Pt A):40-48. doi:
10.1016/j.pnpbp.2016.04.013. Epub 2016 May 3.
Dynamic cross-talk between microglia and peripheral monocytes underlies
stress-induced neuroinflammation and behavioral consequences.
Wohleb ES(1), Delpech JC(2).
(1)Department of Psychiatry, Yale University School of Medicine, USA. Electronic
(2)Department of Psychiatry, Yale University School of Medicine, USA.
Psychological stress promotes the development and recurrence of anxiety and
depressive behavioral symptoms. Basic and clinical research indicates that stress
exposure can influence the neurobiology of mental health disorders through
dysregulation of neuroimmune systems. Consistent with this idea several studies
show that repeated stress exposure causes microglia activation and recruitment of
peripheral monocytes to the brain contributing to development of anxiety- and
depressive-like behavior. Further studies show that stress-induced
re-distribution of peripheral monocytes leads to stress-sensitized neuroimmune
responses and recurrent anxiety-like behavior. These stress-associated immune
changes are important because brain resident and peripheral immune cells
contribute to physiological processes that support neuroplasticity. Thus,
perturbations in neuroimmune function can lead to impaired neuronal responses and
synaptic plasticity deficits that underlie behavioral symptoms of mental health
disorders. In this review we discuss recent advances in neuroimmune regulation of
behavior and summarize studies showing that stress-induced microglia activation
and monocyte trafficking in the brain contribute to the neurobiology of mental
Copyright © 2016 Elsevier Inc. All rights reserved.
PMID: 27154755 [Indexed for MEDLINE]