Abstract
Monoaminergic neurotransmission is a key element in the physiopathology of depressive disorders, but information is still sparse on animal models of this disease. Here, we used the olfactory bulbectomy (OBX) model of depression to characterize cAMP-second messenger signaling pathways, i.e., adenylyl cyclase activity (basal, sodium fluoride (NaF)- and forskolin-stimulated conditions) as well as Gi and Gs protein levels in different regions of the limbic system. Two weeks after surgery and compared to sham controls, OBX rats displayed reduced NaF-stimulated adenylyl cyclase activity and increased Gi/Gs ratios in the hypothalamus, pre-frontal and cingulate cortices but not in the amygdala, hippocampus and caudate nucleus. No differences were found in basal or forskolin-stimulated conditions. The observed reduction of adenylyl cyclase activity induced by NaF and the increase in the Gi/Gs ratio could explain the changes in neurotransmission in OBX rats as well as in humans with depression.
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Effect of fluorosis on mice learning and memory behaviors and brain SOD activity and MDA content
Objective: Explore the brain mechanism of the effect of fluorosis on learning and memory behavior. Method: A method combining behavioral observation and biochemical testing was used to study the effects of long-term drinking different concentrations of sodium fluoride on mouse learning and memory behavior and changes in content of brain
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[Studies on fluoride concentration and cholinesterase activity in rat hippocampus].
OBJECTIVE: To study the accumulation of fluoride in rat hippocampus and its effect on cholinesterase activity. METHODS: Rats were subchronically exposed to NaF, and fluoride concentration and cholinesterase activity in rat hippocampus were determined. RESULTS: Fluoride concentration in rat hippocampus was significantly correlated with the dosage of fluoride, and there
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JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells.
Abstract Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS
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Role of triphala on fluoride neuorotoxicity in the rat
To investigate effects of sodium fluoride (NaF) on the cerebellum cerebral hemisphere brain of rats and its possible amelioration by the popular Ayurvedic herbal health product triphala, adult female Wistar rats (Rattus novergicus) were administered 10 mg NaF/kg bw/day and 30 mg triphala/kg bw/day for 30 days. A significant decline in body and brain
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Protective effects of selenium on fluoride induced alterations in certain enzymes in brain of mice
This study reports the protective effects of selenium on fluoride induced alterations in the activities of pro-oxidative (xanthine oxidase (XOD), lipid peroxidation (LPO) free radical scavenging, [catalase, superoxide dismutase (SOD), glutathione-s-transferase (GST), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione) and metabolic (glucose-6-phosphate dehydrogenase, alanine amino transferase (ALAT), aspartate aminotransferase (AAT),
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Fluoride Affects Learning & Memory in Animals
An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out
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Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects
The NRC's analysis on fluoride and the brain.
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