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
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fulltext
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Title ( eng ) |
Prenatal Exposure to Tributyltin Decreases GluR2 Expression in the Mouse Brain
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Creator |
Ishida Keishi
Saiki Takashi
Umeda Kanae
Miyara Masatsugu
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Source Title |
Biological and Pharmaceutical Bulletin
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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.
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Keywords |
tributyltin
glutamate receptor 2
developmental neurotoxicity
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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.).
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NDC |
Medical sciences [ 490 ]
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Language |
eng
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Resource Type | journal article |
Publisher |
The Pharmaceutical Society of Japan
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Date of Issued | 2017-07-01 |
Rights |
© 2017 The Pharmaceutical Society of Japan
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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
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