Subchronic fluoride intake induces impairment in habituation and active avoidance tasks in rats

Chioca, Lea Rosa; Raupp, Inara; Cunha, Cláudio Da; Losso, Estela Maris; Andreatini, Roberto

doi:10.1016/j.ejphar.2007.10.019

Cited by 52 publications

(30 citation statements)

References 30 publications

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“…In the present study, 30 days of sodium fluoride administration to rats impaired the retention of a habituation memory, which agreed with our previous findings (Chioca et al 2008). Moreover, these behavioural data are Table 1 Mean daily fluid, food and sodium fluoride consumption and degree of dental fluorosis (incisors teeth) of rats treated with water (45 days; W ?…”

Section: Discussionsupporting

confidence: 94%

“…However, only female Wistar rats showed impairment in habituation to a novel object (Bera et al 2007). In agreement with NaF-induced memory impairment, Chioca et al (2008) observed that chronic NaF intake (100 ppm in drinking water for 30 days) impaired open-field habituation and two-way active avoidance of male Wistar rats (Chioca et al 2008).…”

Section: Introductionmentioning

confidence: 70%

“…The open field was cleaned with a 10% alcohol/ water solution prior to behavioural testing to avoid possible bias due to odours and/or residues left by previously tested rats. Twenty-four hours later, a second session, procedurally identical to the training session, was performed (Mello e Souza et al 2000;Chioca et al 2008). The decrease in the number of squares crossed in the second session was taken as a measure of memory retention (Vianna et al 2000;Degroot et al 2005;Pedrazza et al 2007), while a decrease during the test session was taken as a measure of within habituation (Carey et al 1998;Degroot et al 2005).…”

Section: Open-field Testmentioning

confidence: 99%

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Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

et al. 2009

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Previous studies suggest that sodium fluoride (NaF) can impair performance in some memory tasks, such as open-field habituation and two-way active avoidance. In the present study, we evaluated the effect of NaF intake (100 ppm in drinking water for 30 days) and its short-term (15 days) withdrawal on open-field habituation and brain monoamine level. Adult male rats were allocated to three groups: tap water (NaF 1.54 ppm) for 45 days (control group); 15 days of tap water followed by NaF for 30 days; and NaF for 30 days followed by 15 days of tap water. The results showed that NaF impairs open-field habituation and increases noradrenaline (NA) and serotonin (5-HT) in the striatum, hippocampus and neocortex. Dopamine (DA) increase was restricted to the striatum. Short-term NaF withdrawal did not reverse these NaF-induced changes, and both NaF treatments led to a mild fluorosis in rat incisors. No treatment effect was seen in body weight or fluid/water consumption. These results indicate that sodium fluoride induces memory impairment that outlasts short-term NaF withdrawal (2 weeks) and may be associated with NA and 5-HT increases in discrete brain regions.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 70%

Section: Open-field Testmentioning

confidence: 99%

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Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

et al. 2009

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“…Psychiatric symptoms such as lethargy, memory and concentration impairment, and thinking difficulties appeared after chronic exposure to industrial fluoride in workers [5]. In the animal experiments, fluoride decreased the number of avoidance responses in the active avoidance task in rats and had potentially deleterious effects on learning and memory [6]. The learning abilities and memory of high-fluoride exposure mice were significantly lower than those of the control group [7].…”

Section: Introductionmentioning

confidence: 98%

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Yan

Liu

et al. 2015

Mol Neurobiol

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Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about effects on microglia of fluoride. In the present study, healthy adult Wistar rats were exposed to 60 and 120 ppm fluoride in drinking water for 10 weeks, and control rats received deionized water. After 10 weeks, rats were sacrificed under anesthesia then apoptosis in neuron and inflammatory factors secreted by microglia were determined. We found that apoptosis of neurons in fluoride-treated rat brain increased and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive immunofluorescence increased with increasing fluoride concentrations. Bax protein expression increased and Bcl-2 protein expression decreased in fluoride-treated rat brain compared with that of the control rat brain. The microglia in the hippocampus and cortex of fluoride-treated rats were activated by immunostaining with OX-42, a marker of activated microglia, and OX-42-positive microglia cells were more abundant in the hippocampus than in the cortex. The levels of IL-1β and IL-6 protein expression in OX-42-labeled microglial cells were significantly increased in the cortex and hippocampus of rats exposed to fluoride, and TNF-α immunoreactivity in microglial cells of the hippocampus was significantly higher in the 120 ppm fluoride-treated group than that in the control group. Our results indicate that fluoride induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain.

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“…The active avoidance protocol used was a variation of one described previously (Chioca et al, 2008). The mice were allowed a 3-min habituation period, after which they were subjected to seven trials.…”

Section: Active and Passive Avoidance Learningmentioning

confidence: 99%

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice

et al. 2011

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Several studies have suggested a close interaction between serotonin (5-HT) and BDNF; however, little is known of the specific relationship between BDNF and the 5-HT(2C) receptor. Therefore, in this study we investigated BDNF expression in 5-HT(2C) receptor knockout mice (5-HT(2C) KO). We also assessed functional consequences of any changes in BDNF using a behavioral test battery. Western blot analysis demonstrated a significant 2.2-fold increase in the expression of the mature form of BDNF in 5-HT(2C) KO mice when compared with wild-type controls (WT) in the hippocampus (P = 0.008), but not frontal cortex or striatum. No differences in the expression of the pro-BDNF isoform were found, and the ratio of mature/pro BDNF was significantly increased in 5-HT(2C) KO (P = 0.003). BDNF mRNA expression in the hippocampus was not different between the genotypes. Hence, increased mature BDNF levels in 5-HT(2C) KO hippocampus are most likely due to increased extracellular cleavage rates of pro-BDNF to its mature form. Protein expression of the BDNF receptor, tropomycin-related receptor B (TrkB), was also unchanged in the hippocampus, frontal cortex and striatum. With repeated training in a 10-day win-shift radial arm maze task, 5-HT(2C) KO and WT showed similar decreases of the number of working memory and reference memory errors. In addition, no genotype specific differences were observed for passive or active avoidance learning. 5-HT(2C) KO showed modest locomotor hyperactivity but no differences in tests for anxiety, sensorimotor gating, or depressive-like behaviors; however, in the tail suspension test 5-HT(2C) KO showed significantly reduced climbing (P < 0.05). In conclusion, loss of 5-HT(2C) receptor expression leads to a marked and selective increase in levels of the mature form of BDNF in the hippocampus. Despite this marked increase, 5-HT(2C) KO show only subtle behavioral changes.

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Subchronic fluoride intake induces impairment in habituation and active avoidance tasks in rats

Cited by 52 publications

References 30 publications

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice

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Subchronic fluoride intake induces impairment in habituation and active avoidance tasks in rats

Cited by 52 publications

References 30 publications

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT2C receptor knockout mice

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Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice