From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival

Abstract

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.

The role of teratogens in neural crest development

“…A decrease in the expression of EMT‐related adhesion molecules ( Cad6B , E‐Cadherin , and N‐cadherin ) in the NC was also observed. In agreement with these findings, imidacloprid reduced the expression of Shh and Bmp4 in the chick neural tube, with a failure of neural tube closure (Liu et al, ). Imidacloprid affects the thyroid follicles, pituitary gland, estrogen, and also has an adipogenic effect on birds (Pandey & Mohanty, ).…”

The Neonicotinoid Thiacloprid Interferes with the Development, Brain Antioxidants, and Neurochemistry of Chicken Embryos and Alters the Hatchling Behavior: Modulatory Potential of Phytochemicals

“…Goyal et al reported that TH induced neurological disorders in Gallus domesticus associated with brain histopathological changes [ 56 ]. Similarly, imidacloprid treatment inhibited both AChE and acetylcholine receptors, negatively affected neurogenesis during embryonic development of chicks, reduced cell proliferation, increased cell apoptosis, and altered the brain histoarchitecture [ 57 ].…”

An update of the Worldwide Integrated Assessment (WIA) on systemic insecticides. Part 2: impacts on organisms and ecosystems

“…Imidacloprid and fipronil had deleterious effects on growth of birds, exhibited as growth retardation, reduced weight gain and lost body condition, often as a consequence of reduced food intake (Hussein et al 2014a, b;Khalil et al 2017;LopezAntia et al 2015b). During embryonic development of birds, exposure to imidacloprid caused heart malformation , neural tube defects (Liu et al 2016;Wang et al 2016b), altered organ mass, and other anatomical deformities (Gobeli et al 2017). In red-legged partridges, exposure to imidacloprid led to a depressed immune response in offspring of treated parents (Lopez-Antia et al 2015a) and of parents and offspring when exposed to fipronil (Lopez-Antia et al 2015b).…”