Title: | Fluoride-induced alterations of synapse-related proteins in the cerebral cortex of ICR offspring mouse brain |
Author(s): | Ge Y; Chen L; Yin Z; Song X; Ruan T; Hua L; Liu J; Wang J; Ning H; |
Address: | "College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, Henan, 453003, PR China. College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, Henan, 453003, PR China; Shanxi Key Laboratory of Ecological Animal Science and Environmental Medicine, Shanxi Agricultural University, Taigu, Shanxi, 030801, PR China. College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, PR China. Shanxi Key Laboratory of Ecological Animal Science and Environmental Medicine, Shanxi Agricultural University, Taigu, Shanxi, 030801, PR China. Electronic address: wangjd@sxau.edu.cn. College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, Henan, 453003, PR China; Shanxi Key Laboratory of Ecological Animal Science and Environmental Medicine, Shanxi Agricultural University, Taigu, Shanxi, 030801, PR China. Electronic address: pangpangning@126.com" |
DOI: | 10.1016/j.chemosphere.2018.02.167 |
ISSN/ISBN: | 1879-1298 (Electronic) 0045-6535 (Linking) |
Abstract: | "Fluoride (F) exposure causes cognitive dysfunction in humans and animals. However, the precise molecular mechanisms by which fluoride exerts its neurotoxic effects are poorly understood. In this study, an animal model of fluoride exposure was created by providing ICR mice were treated with vehicle F at a dose of 0 (control group), 50 (low-fluoride group) or 100?ª+mg/L (high-fluoride group) in water for one month. After the mice mated, parents and offspring were treated and maintained under these conditions. The cognitive abilities of the mice were examined using a Morris water maze test. Results indicated that fluoride exposure significantly prolonged the escape latency period and decreased the number of crossings in a particular zone. Histopathologic analysis revealed the shrinkage and fragmentation of glial cells in the fluoride-treated groups. Pyramidal cells in the cerebral cortices of fluoride-treated groups were fewer than those of the control group. The expression of microtubule-associated protein 2 (MAP2) and synaptic proteins of the cerebral cortex in mouse offspring was assayed using RT-PCR and Western blot. Fluoride exposure possibly induced a significantly decreased expression of MAP2, synaptophysin (SYP) and developmentally regulated brain protein (Dbn) at protein and mRNA levels. Glutamate receptor (N-methyl-d-aspartate receptor, NMDAR) was also expressed, and this finding was consistent with the reduced MAP2, SYP and Dbn expression. Therefore, fluoride-mediated reduction in cognitive dysfunction is likely caused by the disruption of the expression of these synapse-associated proteins, resulting in attenuated neuronal functioning" |
Keywords: | "Animals Behavior, Animal/drug effects Cerebral Cortex/*drug effects/metabolism/pathology Environmental Pollutants/*toxicity Female Fluorides/*toxicity Male Maze Learning/drug effects Mice, Inbred ICR Microtubule-Associated Proteins/metabolism Nerve Tissue;" |
Notes: | "MedlineGe, Yaming Chen, Lingli Yin, Zhihong Song, Xiaochao Ruan, Tao Hua, Liushuai Liu, Junwei Wang, Jundong Ning, Hongmei eng England 2018/03/24 Chemosphere. 2018 Jun; 201:874-883. doi: 10.1016/j.chemosphere.2018.02.167. Epub 2018 Feb 27" |