Citation

Weber MD, Godbout JP, Sheridan JF. Neuropsychopharmacology 2016; 42(1): 46-61.

Affiliation

Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH.

Copyright

(Copyright © 2016, Nature Publishing Group)

DOI

10.1038/npp.2016.102

PMID

27319971

Abstract

Mounting evidence indicates that pro-inflammatory signaling in the brain affects mood, cognition, and behavior and is linked with the etiology of psychiatric disorders, including anxiety and depression. The purpose of this review is to focus on stress-induced bi-directional communication pathways between the CNS and peripheral immune system that converge to promote a heightened neuroinflammatory environment. These communication pathways involve sympathetic outflow from the brain to the peripheral immune system that biases hematopoietic stem cells to differentiate into a glucocorticoid resistant and primed myeloid lineage immune cell. In conjunction, microglia-dependent neuroinflammatory events promote myeloid cell trafficking to the brain that reinforces stress-related behavior, and is argued to play a role in stress-related psychiatric disorders. We will discuss evidence implicating a key role for endothelial cells that comprise the blood brain barrier in propagating peripheral-to-central immune communication. We will also discuss novel neuron-to-glia communication pathways involving endogenous danger signals that have recently been argued to facilitate neuroinflammation under various conditions, including stress. These findings help elucidate the complex communication that occurs in response to stress and highlights novel therapeutic targets against the development of stress-related psychiatric disorders.Neuropsychopharmacology accepted article preview online, 20 June 2016. doi:10.1038/npp.2016.102.

Language: en