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Polybrominated diphenyl ethers (PBDEs) can induce neurotoxicity, but the mechanism of their toxicity on the cholinergic system and locomotion behavior remains unclear. In this paper, zebrafish embryos were exposed to DE-71 (0, 1, 3, 10, 30, and 100 µg/L) until 120 h post fertilization, and its effects on the behavior and cholinergic system of zebrafish larvae and its possible mechanism were investigated. Results indicated a general locomotor activity impairment in the light-dark transition stimulation without affecting the secondary motoneurons. However, with the extension of test time in the dark or light, the decreased locomotor activity was diminished, a significant decrease only observed in the 100 µg/L DE-71 exposure groups in the last 10 min. Furthermore, whole-body acetylcholine (ACh) contents decreased after DE-71 exposure, whereas no changes in NO contents and inducible nitric oxide synthase activity were found. The expression of certain genes encoding calcium homeostasis proteins (e.g., grin1a, camk2a, and crebbpb) and the concentrations of calcium in zebrafish larvae were significantly decreased after DE-71 exposure. After co-exposure with calcium channel agonist (±)-BAY K8644, calcium concentrations, ACh contents, and locomotor activity in the light-dark transition stimulation was significantly increased compared with the same concentrations of DE-71 exposure alone, whereas no significant difference was observed compared with the control, indicating that calcium homeostasis is involved in the impairment of cholinergic neurotransmission and locomotor activity. Overall, our results suggested that DE-71 can impair the cholinergic system and locomotor activity by impairing calcium homeostasis. Our paper provides a better understanding of the neurotoxicity of PBDEs. |
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