Abstract
In order to reveal the mechanism of the decreased ability of learning and memory induced by chronic fluorosis, nicotinic acetylcholine receptors (nAChRs) and the pathway of extracellular signal regulated protein kinase (ERK1/2) were investigated by using the rats fed with different concentrations of sodium fluoride for 6 months. Spatial learning and memory of the rats were evaluated by Morris Water Maze test. The expressions of nAChRs, ERK1/2 and mitogen-induced extracellular kinase (MEK1/2) at protein and mRNA levels were detected by Western blotting and real-time PCR, respectively. The results showed that as compared with controls, the learning and memory capacity in the rats with fluorosis was decreased. The protein expressions of alpha7 and alpha4 nAChR subunits in rat brains with fluorosis were decreased by 35% and 33%, whereas the corresponding receptor subunit mRNAs did not exhibit any changes. The increases of phospho- and total-ERK1/2 as well as phospho-MEK1/2 at the protein levels were found in the brains of rats with fluorosis as compared to controls, and no difference of ERK1/2 mRNA was found. In addition, the activation rate of phospho-ERK1/2 was decreased in the brains affected with fluorosis. The modifications of nAChRs and ERK1/2 pathway might be connected with the molecular mechanisms in the decreased capacity of learning and memory of the rats with fluorosis.
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Changes of learning and memory ability and brain nicotinic receptors of rat offspring with coal burning fluorosis.
The purpose of the investigation is to reveal the mechanism of the decreased ability of learning and memory induced by coal burning fluorosis. Ten offspring SD rats aged 30days, who were born from the mothers with chronic coal burning fluorosis, and ten offspring with same age from the normal mothers
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Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the a7 nicotinic receptor and oxidative stress.
Daily exposure to fluoride (F) depends mainly on the intake of this element with drinking water. When administered during gestation and lactation, F has been associated with cognitive deficits in the offspring. However, the mechanisms underlying the neurotoxicity of F remain obscure. In the current study, we investigated the effects
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The effect of fluorine exposure of pregnant rats on the learning and memory capabilities of baby rats
Objective: Explore the effect and possible mechanisms of fluorine exposure of pregnant rats passing through placental barriers on the learning and memory capabilities of baby rats. Method: Open field behavior and a water maze test were used to observe the effects on the spontaneous behavior and learning and memory on baby
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ERK1/2-mediated disruption of BDNF–TrkB signaling causes synaptic impairment contributing to fluoride–induced developmental neurotoxicity
Highlights Rats were long–term chronic exposed to environmentally relevant doses of fluoride. Fluoride exposure results in synaptic alterations both in vivo and in vitro. Fluoride–induced cognitive failures correlates with synaptic deficits. BDNF–TrkB axis disruption contributes to fluoride–elicited impaired synaptogenesis. ERK1/2 plays a vital role in fluoride–induced BDNF–TrkB signaling disruption. Excessive
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[The establishment and assessment of animal model of chronic fluorosis-induced cognitive dysfunction in rats].
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
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