Low level prenatal exposure to methylmercury disrupts neuronal migration in the developing rat cerebral cortex
文献类型:期刊论文
作者 | Guo, BQ ; Yan, CH ; Cai, SZ ; Yuan, XB ; Shen, XM |
刊名 | TOXICOLOGY
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出版日期 | 2013 |
卷号 | 304页码:57-68 |
关键词 | CELL-CYCLE KINETICS CORTICAL-NEURONS DEVELOPING BRAIN DEVELOPMENTAL NEUROTOXICITY PROTEASOME SYSTEM IN-VIVO MERCURY EXPRESSION UBIQUITIN RHO |
ISSN号 | 0300-483X |
通讯作者 | Yan, CH (reprint author), Shanghai Jiao Tong Univ, Sch Med, XinHua Hosp, MOE Shanghai Key Lab Childrens Environm Hlth, 1665 Kong Jiang Rd, Shanghai 200092, Peoples R China.,yanch@shkeylab-ceh.org |
英文摘要 | We determined the effects of low-level prenatal MeHg exposure on neuronal migration in the developing rat cerebral cortex using in utero electroporation. We used offspring rats born to dams that had been exposed to saline or various doses of MeHg (0.01 mg/kg/day, 0.1 mg/kg/day, and 1 mg/kg/day) from gestational day (GD) 11-21. Immunohistochemical examination of the brains of the offspring was conducted on postnatal day (PND) 0, PND3, and PND7. Our results showed that prenatal exposure to low levels of MeHg (0.1 mg/kg/day or 1 mg/kg/day) during the critical stage in neuronal migration resulted in migration defects of the cerebrocortical neurons in offspring rats. Importantly, our data revealed that the abnormal neuronal distribution induced by MeHg was not caused by altered proliferation of neural progenitor cells (NPCs), induction of apoptosis of NPCs and/or newborn neurons, abnormal differentiation of NPCs, and the morphological changes of radial glial scaffold, indicating that the defective neuronal positioning triggered by exposure to low-dose of MeHg is due to the impacts of MeHg on the process of neuronal migration itself. Moreover, we demonstrated that in utero exposure to low-level MeHg suppresses the expression of Rac1, Cdc42, and RhoA, which play key roles in the migration of cerebrocortical neurons during the early stage of brain development, suggesting that the MeHg-induced migratory disturbance of cerebrocortical neurons is likely associated with the Rho GTPases signal pathway. In conclusion, our results provide a novel perspective on clarifying the mechanisms underlying the impairment of neuronal migration induced by MeHg. (C) 2012 Elsevier Ireland Ltd. All rights reserved. |
学科主题 | Pharmacology & Pharmacy ; Toxicology |
收录类别 | SCI |
资助信息 | National Natural Science Foundation of China [30872806]; Public Welfare Project of the Chinese Ministry of Health [201002001, 201002006]; National Basic Research Program of China (973 Program) [2012CB525001] |
语种 | 英语 |
公开日期 | 2013-06-04 |
源URL | [http://ir.sibs.ac.cn/handle/331001/2521] ![]() |
专题 | 上海神经科学研究所_神经所(总) |
推荐引用方式 GB/T 7714 | Guo, BQ,Yan, CH,Cai, SZ,et al. Low level prenatal exposure to methylmercury disrupts neuronal migration in the developing rat cerebral cortex[J]. TOXICOLOGY,2013,304:57-68. |
APA | Guo, BQ,Yan, CH,Cai, SZ,Yuan, XB,&Shen, XM.(2013).Low level prenatal exposure to methylmercury disrupts neuronal migration in the developing rat cerebral cortex.TOXICOLOGY,304,57-68. |
MLA | Guo, BQ,et al."Low level prenatal exposure to methylmercury disrupts neuronal migration in the developing rat cerebral cortex".TOXICOLOGY 304(2013):57-68. |
入库方式: OAI收割
来源:上海神经科学研究所
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