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Published on: November 17, 2017
Fluoride-induced alterations of synapse-related proteins in the cerebral cortex of ICR offspring mouse brain
Yaming Ge1, Lingli Chen2, Zhihong Yin1
1College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, Henan, 453003, PR China.
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 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.
Insights
Fluoride exposure impairs cognitive function by reducing key synapse-associated proteins in the brain. This neurotoxicity affects neuronal functioning and learning abilities in offspring.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Fluoride exposure is linked to cognitive dysfunction, but its molecular mechanisms remain unclear.
- Understanding fluoride's neurotoxic effects is crucial for public health.
- Previous studies suggest potential impacts on brain function.
Purpose of the Study:
- To investigate the molecular mechanisms of fluoride-induced neurotoxicity.
- To examine the effects of fluoride exposure on cognitive function and synaptic protein expression in mice.
- To assess the impact on both parent and offspring generations.
Main Methods:
- Created an animal model using ICR mice exposed to varying fluoride concentrations (0, 50, 100 mg/L) in drinking water.
- Assessed cognitive abilities using the Morris water maze test.
- Analyzed brain tissue for histopathological changes and quantified protein and mRNA expression of microtubule-associated protein 2 (MAP2), synaptophysin (SYP), and developmentally regulated brain protein (Dbn) using RT-PCR and Western blot.
Main Results:
- Fluoride exposure significantly prolonged escape latency and reduced crossings in the Morris water maze, indicating cognitive impairment.
- Histopathological analysis showed glial cell shrinkage, fragmentation, and reduced pyramidal cells in the cerebral cortex.
- A significant decrease in MAP2, SYP, and Dbn expression at both protein and mRNA levels was observed in fluoride-exposed offspring.
Conclusions:
- Fluoride exposure disrupts the expression of crucial synapse-associated proteins (MAP2, SYP, Dbn), leading to cognitive dysfunction.
- The observed neurotoxicity is associated with attenuated neuronal functioning and potential N-methyl-d-aspartate receptor (NMDAR) alterations.
- These findings highlight the detrimental impact of fluoride on cognitive development and neuronal integrity.
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