Social defeat stress induces phosphorylation of extracellular signal‐regulated kinase in the leptomeninges in mice. Issue 2 (14th February 2019)

• Record Type: Journal Article
• Authors: Okamura, Satoshi; Nagai, Hirotaka; Numa, Chisato; Nagai, Midori; Shinohara, Ryota; Furuyashiki, Tomoyuki
• Is Part Of: Neuropsychopharmacology reports. Volume 39:Issue 2(2019)
• Page Start: 134
• Page End: 139
• Publication Date: 2019-02-14
• Subjects: depression -- inflammation -- MAP Kinase -- meninges -- psychological stress; Neuropsychopharmacology -- Periodicals; 615.78
• DOI: 10.1002/npr2.12051
• Languages: English
• ISSNs: 2574-173X

Abstract

Abstract : Aims: Animal studies using various stress models have shown that excessive environmental stress induces depression? and anxiety?like behaviors through inflammatory responses in the brain and periphery. Although the leptomeningeal cells have multiple functions related to inflammatory responses in the brain, whether environmental stress influences the leptomeninges remains unknown. In this study, we aimed to examine phosphorylation of the extracellular signal‐regulated kinase (ERK) in the leptomeninges. Methods: We subjected C57BL/6 male mice to a single episode of social defeat stress and analyzed the expression of phosphorylated ERK in the leptomeninges by immunohistochemistry. Results: Social defeat stress in mice induced phosphorylation of ERK in the leptomeninges, adjacent to vascular endothelial cells and the glia limitans. This ERK phosphorylation was maintained for at least one hour after the stress. Conclusions: This study shows the effect of environmental stress on the leptomeninges for the first time and paves the way for elucidating its functional role in stress‐induced changes in neural functions. Abstract : This study shows for the first time that social defeat stress induces phosphorylation of extracellular signal‐regulated kinase in the leptomeninges in mice. This finding paves the way for elucidating a potential role of the leptomeninges in mediating stress‐induced inflammatory signals from the periphery to the brain.