TNF-α from hippocampal microglia induces working memory deficits by acute stress in mice

Masahiro Ohgidani, Takahiro A. Kato, Noriaki Sagata, Kohei Hayakawa, Norihiro Shimokawa, Mina Sato-Kasai, Shigenobu Kanba

研究成果: Contribution to journalArticle査読

40 被引用数 (Scopus)

抄録

The role of microglia in stress responses has recently been highlighted, yet the underlying mechanisms of action remain unresolved. The present study examined disruption in working memory due to acute stress using the water-immersion resistant stress (WIRS) test in mice. Mice were subjected to acute WIRS, and biochemical, immunohistochemical, and behavioral assessments were conducted. Spontaneous alternations (working memory) significantly decreased after exposure to acute WIRS for 2 h. We employed a 3D morphological analysis and site- and microglia-specific gene analysis techniques to detect microglial activity. Morphological changes in hippocampal microglia were not observed after acute stress, even when assessing ramification ratios and cell somata volumes. Interestingly, hippocampal tumor necrosis factor (TNF)-α levels were significantly elevated after acute stress, and acute stress-induced TNF-α was produced by hippocampal-ramified microglia. Conversely, plasma concentrations of TNF-α were not elevated after acute stress. Etanercept (TNF-α inhibitor) recovered working memory deficits in accordance with hippocampal TNF-α reductions. Overall, results suggest that TNF-α from hippocampal microglia is a key contributor to early-stage stress-to-mental responses.

本文言語英語
ページ(範囲)17-24
ページ数8
ジャーナルBrain, Behavior, and Immunity
55
DOI
出版ステータス出版済み - 7 1 2016

All Science Journal Classification (ASJC) codes

  • 免疫学
  • 内分泌系および自律システム
  • 行動神経科学

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