Okamura Satoshi, Nagai Hirotaka, Numa Chisato, Nagai Midori, Shinohara Ryota, Furuyashiki Tomoyuki
Division of Pharmacology, Graduate School of Medicine, Kobe University, Kobe, Japan.
Neuropsychopharmacol Rep. 2019 Jun;39(2):134-139. doi: 10.1002/npr2.12051. Epub 2019 Feb 14.
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.
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.
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.
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.
使用各种应激模型的动物研究表明，过度的环境应激通过大脑和外周的炎症反应诱发抑郁样和焦虑样行为。尽管软脑膜细胞具有多种与大脑炎症反应相关的功能，但环境应激是否会影响软脑膜仍不清楚。在本研究中，我们旨在检测软脑膜中细胞外信号调节激酶（ERK）的磷酸化情况。
我们让C57BL/6雄性小鼠经历单次社会挫败应激，并通过免疫组织化学分析软脑膜中磷酸化ERK的表达。
小鼠的社会挫败应激诱导了软脑膜中ERK的磷酸化，其位于血管内皮细胞和胶质界膜附近。这种ERK磷酸化在应激后至少持续一小时。
本研究首次展示了环境应激对软脑膜的影响，为阐明其在应激诱导的神经功能变化中的功能作用铺平了道路。
