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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Proteomic analysis of hippocampus in offspring male mice exposed to fluoride and lead
Fluoride and lead are two common pollutants in the environment. Previous investigations have found that high fluoride exposure can increase the lead burden. In this experiment, in order to study on the molecular mechanisms of central neural system injury induced by the above two elements, differently expressed protein spots in
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Neonatal sevoflurane anesthesia induces long-term memory impairment and decreases hippocampal PSD-95 expression without neuronal loss.
AIM: Volatile anesthetics are widely used in the clinic, and sevoflurane is the most prevalent volatile anesthetic in pediatric anesthesia. Recent findings question the potential risks of volatile anesthetics on brain development. Evidence suggests that sevoflurane may cause neuronal deficiency. This study investigates the long-term effect of sevoflurane in the
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Molecular mechanism of brain impairment caused by drinking-acquired fluorosis and selenium intervention
This study investigated the molecular mechanism of brain impairment induced by drinking fluoridated water and selenium intervention. Results showed that the learning and memory of rats in NaF group significantly decreased. Moreover, the number of apoptotic cells, the expression levels of Cytc mRNA and protein, and the expression levels of
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Pathologic changes and effect on the learning and memory ability in rats exposed to fluoride and aluminum
Background: The aim of this study is to establish a single and combined intoxication model of fluoride and aluminum so as to observe the impact of these chemicals on the learning and memory ability and the pathologic changes in brain of rats. Methods: Forty male Wistar rats were randomly assigned
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MiR-132, miR-204 and BDNF-TrkB signaling pathway may be involved in spatial learning and memory.
Highlights Spatial learning and memory of offspring rats were impaired after exposure to fluorine combined with aluminium(FA). Hippocampal miR-132 and miR-204 were increased after FA exposure. Hippocampal BDNF-TrkB signaling pathway was down-regulated after FA exposure. There were antagonistic effects between F and Al, with Al reducing the toxicity of F. Fluorine
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Fluoride Affects Learning & Memory in Animals
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
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Fluoride's Direct Effects on Brain: Animal Studies
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Fluoride & IQ: 67 Studies
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