Abstract
Objective To establish the rat model of cognitive dysfunction induced by chronic fluorosis and to investigate the underlying mechanism.
Methods Animal model of chronic fluorosis was established by feeding Wistar rats on distillated water containing different concentrations of sodium fluoride (0, 50, 100, and 150 mg/L) for six months; Y-maze and open field test were used to evaluate the changes in cognitive ethology of rats; the morphological changes of rat hippocampus were observed using H-E staining.
Results The learning and memory abilities were lower in chronic fluorosis groups, particularly in medium and high fluorosis groups (P <0.05 or P <0.01) than in the normal group. Compared with the normal group, marked morphological changes were observed in the hippocampal cells in high fluorosis group.
Conclusion The rat model has a strong resemblance in cognitive dysfunction caused by chronic fluorosis to that in population of high fluorosis areas, which is available to serve as an animal model to study the cognitive impairment caused by chronic fluorosis.
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Attenuating effect of Vitamin E on the deficit of learning and memory of rats with chronic fluorosis: the mechanism may involve muscarinic acetylcholine receptors.
The protective role of vitamin E (Vit E) against neurotoxicity induced by fluorosis was investigated by using Sprague-Dawley (SD) rats fed with 50 ppm fluoride in drinking water for 10 months. Spatial learning and memory of rats were measured by the Morris water maze test; the expressions of M1 and
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Decreased learning ability and low hippocampus glutamate in offspring rats exposed to fluoride and lead.
Fluoride (F) and lead (Pb) are two common environmental pollutants which are linked to the lowered intelligence, especially for children. Glutamate, a major excitatory neurotransmitter in the central nervous system, plays an important role in the process of learning and memory. However, the impact of F and Pb alone or
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Gestational exposure to fluoride impairs cognition in C57 BL/6 J male offspring mice via the p-Creb1-BDNF-TrkB signaling pathway.
Highlights Pregnant mice were exposed to environmentally relevant doses of sodium fluoride from GD1 to GD20. Exposure to sodium fluoride resulted in structural and functional impairments in male offspring mouse hippocampus. The activation of P-Creb1 signaling pathway played a role in sodium fluoride-induced cognitive impairment. We provided new insight
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Roles of mitochondrial fission inhibition in developmental fluoride neurotoxicity: mechanisms of action in vitro and associations with cognition in rats and children.
Fluoride neurotoxicity is associated with mitochondrial disruption. Mitochondrial fission/fusion dynamics is crucial to maintain functional mitochondria, yet little is known about how fluoride perturbs this dynamics and whether such perturbation contributes to impaired neurodevelopment. Here in human neuroblastoma SH-SY5Y cells treated with sodium fluoride (NaF, 20, 40 and 60 mg/L), mitochondrial
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Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice.
SUMMARY: Learning-memory behavior was tested in mice on a Y-maze after they drank water containing different concentrations of sodium fluoride. Impairment of the structure of the Gray I synaptic interface in the CA3 area of the hippocampus was analyzed quantitatively by electron microscopy and a computer imaging processor. The main
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