Prenatal Exposure to Tributyltin Decreases GluR2 Expression in the Mouse Brain

Biological and Pharmaceutical Bulletin Volume 40 Issue 7 Page 1121-1124 published_at 2017-07-01
アクセス数 : 677
ダウンロード数 : 220

今月のアクセス数 : 1
今月のダウンロード数 : 1
File
BiolPhamBull_40_1121.pdf 4.6 MB 種類 : fulltext
Title ( eng )
Prenatal Exposure to Tributyltin Decreases GluR2 Expression in the Mouse Brain
Creator
Ishida Keishi
Saiki Takashi
Umeda Kanae
Miyara Masatsugu
Source Title
Biological and Pharmaceutical Bulletin
Volume 40
Issue 7
Start Page 1121
End Page 1124
Abstract
Tributyltin (TBT), a common environmental contaminant, is widely used as an antifouling agent in paint. We previously reported that exposure of primary cortical neurons to TBT in vitro decreased the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit glutamate receptor 2 (GluR2) expression and subsequently increased neuronal vulnerability to glutamate. Therefore, to identify whether GluR2 expression also decreases after TBT exposure in vivo, we evaluated the changes in GluR2 expression in the mouse brain after prenatal or postnatal exposure to 10 and 25 ppm TBT through pellet diets. Although the mean feed intake and body weight did not decrease in TBT-exposed mice compared with that in control mice, GluR2 expression in the cerebral cortex and hippocampus decreased after TBT exposure during the prenatal period. These results indicate that a decrease in neuronal GluR2 may be involved in TBT-induced neurotoxicity, especially during the fetal period.
Keywords
tributyltin
glutamate receptor 2
developmental neurotoxicity
Descriptions
This study was supported by JSPS KAKENHI (B) Grant Numbers 23310047 (to Y.K.), 15H02826 (to Y.K.), and a Grant-in-Aid for JSPS Fellows Number 14J06534 (to K.I.).
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type journal article
Publisher
The Pharmaceutical Society of Japan
Date of Issued 2017-07-01
Rights
© 2017 The Pharmaceutical Society of Japan
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0918-6158
[ISSN] 1347-5215
[NCID] AA10885497
[DOI] 10.1248/bpb.b17-00209
[DOI] https://doi.org/10.1248/bpb.b17-00209