Exposing imidacloprid interferes with neurogenesis through impacting on chick neural tube cell survival

Meng Liu, Guang Wang, Shi-Yao Zhang, Shan Zhong, Guo-Long Qi, Chao-Jie Wang, Manli Chuai, Kenneth Ka Ho Lee, Da-Xiang Lu, Xuesong Yang (Lead / Corresponding author)

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    As a neonicotinoid pesticide, imidacloprid is widely used to control insects in agriculture and fleas on domestic animals. However, it is not known whether imidacloprid exposure negatively affects neurogenesis during embryonic development. In this study, using a chick embryo model, we investigated the effects of imidacloprid exposure on neurogenesis at the earliest stage and during late-stage embryo development. Exposing HH0 chick embryos to imidacloprid in EC culture caused neural tube defects (NTDs) and neuronal differentiation dysplasia as determined by NF/Tuj1 labeling. Furthermore, we found that F-actin accumulation on the apical side of the neural tube was suppressed by exposure to imidacloprid, and the expression of BMP4 and Shh on the dorsal and ventral sides of the neural tubes, respectively, were also reduced, which in turn affects the dorsolateral hinge points during bending of the neural plate. In addition, exposure to imidacloprid reduced cell proliferation and increased cell apoptosis, as determined by pHIS3 labeling and TUNEL staining, respectively, also contributing to the malformation. We obtained similar results in late-stage embryos exposed to imidacloprid. Finally, a bioinformatics analysis was employed to determine which genes identified in this study were involved in NTDs. The experimental evidence and bioinformatics analysis suggested that imidacloprid exposure during chick embryo development could increase the risk of NTDs and neural dysplasia.

    Original languageEnglish
    Pages (from-to)137-148
    Number of pages12
    JournalToxicological Sciences
    Issue number1
    Early online date21 Jul 2016
    Publication statusPublished - 21 Jul 2016


    • imidacloprid
    • neural tube defect
    • neuronal differentiation
    • cell proliferation/apoptosis
    • EMP4/Shh


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