Host: The Japanese Society of Toxicology
Neonicotinoids are pesticides used the most frequently in Japan. Neonicotinoids act as agonists for the nicotinic acetylcholine receptor (nAchR) and exhibit insecticidal effects by disrupting neurotransmission. Neonicotinoids are considered to bind to only insect nAchR, but the effects of their exposure on mammals should be examined with regard to the similarity between insects and mammalian nAchR. In this study, we aim to investigate the developmental neurotoxicity of neonicotinoids using mice. Imidacloprid (IMI) and clothianidin (CLO) were administered at a dose of 0.1 mg/kg/day from gestational day 11 to postnatal day 21. IMI developmental exposure reduced survival rate 11 days after birth and eye opening was delayed. Abnormal anxiety-like, social and repetitive behaviors were observed after growth. CLO developmental exposure reduced survival rate 15 days after birth and eye opening was also delayed. Anxiety-like, repetitive and depression-like behavior were observed after growth. In the hippocampus of 10-day-old mice, the number of microglia decreased due to developmental exposure to neonicotinoids. The morphology of microglia changed from amoeboid to ramified forms, and the phagocytic ability was reduced, indicating decreased microglial activity by neonicotinoids. Taken together, neonicotinoid developmental exposure can induce abnormal behaviors after growth via decreases in and/or inactivation of microglia during developmental stage.
