ツジ マユミ   Tsuji Mayumi
  辻 真弓
   所属   医学部医学科  基礎医学系 衛生学
   職種   教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Neuroprotective activation of astrocytes by methylmercury exposure in the inferior colliculus.
掲載誌名 正式名:Scientific reports
略  称:Sci Rep
ISSNコード:20452322/20452322
巻・号・頁 9(1),13899頁
著者・共著者 Ishihara Yasuhiro, Itoh Kouichi, Oguro Ami, Chiba Yoichi, Ueno Masaki, Tsuji Mayumi, Vogel Christoph F A, Yamazaki Takeshi
発行年月 2019/09
概要 Methylmercury (MeHg) is well known to induce auditory disorders such as dysarthria. When we performed a global analysis on the brains of mice exposed to MeHg by magnetic resonance imaging, an increase in the T1 signal in the inferior colliculus (IC), which is localized in the auditory pathway, was observed. Therefore, the purpose of this study is to examine the pathophysiology and auditory dysfunction induced by MeHg, focusing on the IC. Measurement of the auditory brainstem response revealed increases in latency and decreases in threshold in the IC of mice exposed to MeHg for 4 weeks compared with vehicle mice. Incoordination in MeHg-exposed mice was noted after 6 weeks of exposure, indicating that IC dysfunction occurs earlier than incoordination. There was no change in the number of neurons or microglial activity, while the expression of glial fibrillary acidic protein, a marker for astrocytic activity, was elevated in the IC of MeHg-exposed mice after 4 weeks of exposure, indicating that astrogliosis occurs in the IC. Suppression of astrogliosis by treatment with fluorocitrate exacerbated the latency and threshold in the IC evaluated by the auditory brainstem response. Therefore, astrocytes in the IC are considered to play a protective role in the auditory pathway. Astrocytes exposed to MeHg increased the expression of brain-derived neurotrophic factor in the IC, suggesting that astrocytic brain-derived neurotrophic factor is a potent protectant in the IC. This study showed that astrogliosis in the IC could be an adaptive response to MeHg toxicity. The overall toxicity of MeHg might be determined on the basis of the balance between MeHg-mediated injury to neurons and protective responses from astrocytes.
DOI 10.1038/s41598-019-50377-9
PMID 31554907