Effect of Prenatal Aluminium Lactate Exposure on Conditioned Taste Aversion and Passive Avoidance Task in the Rat

Gonda, Zsuzsanna; Lehotzky, K

doi:10.1002/(sici)1099-1263(199611)16:6<529::aid-jat392>3.0.co;2-s

Cited by 21 publications

(11 citation statements)

References 2 publications

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“…Al-induced inhibition of the neuronal glutamate-NO-cGMP pathway could result in impaired intercellular communication and altered intracellular signal transduction pathways and could be in the origin of Al neurotoxicity. Inhibition of this pathway can be responsible for Al-induced impairment of long-term potentiation (Platt et al, 1995;Platt and Reyman, 1996) and learning (Gonda and Lehotzky, 1996) and for the neurotoxic and neurobehavioral effects of Al.…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Aluminum Impairs Neuronal Glutamate‐Nitric Oxide‐Cyclic GMP Pathway

Cucarella

Montoliú

Hermenegildo

et al. 1998

Journal of Neurochemistry

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Humans are exposed to aluminum from environmental sources and therapeutic treatments. However, aluminum is neurotoxic and is considered a possible etiologic factor in Alzheimer's disease and other neurological disorders. The molecular mechanism of aluminum neurotoxicity is not understood. We tested the effects of aluminum on the glutamate‐nitric oxide‐cyclic GMP pathway in cultured neurons. Neurons were exposed to 50 µM aluminum in culture medium for short‐term (4 h) or long‐term (8–14 days) periods, or rats were prenatally exposed, i.e., 3.7% aluminum sulfate in the drinking water, during gestation. Chronic (but not short‐term) exposure of neurons to aluminum decreased glutamate‐induced activation of nitric oxide synthase by 38% and the formation of cyclic GMP by 77%. The formation of cyclic GMP induced by the nitric oxide‐generating agent S‐nitroso‐N‐acetylpenicillamine was reduced by 33%. In neurons from rats prenatally exposed to aluminum but not exposed to it during culture, glutamate‐induced formation of cyclic GMP was inhibited by 81%, and activation of nitric oxide synthase was decreased by 85%. The formation of cyclic GMP induced by S‐nitroso‐N‐acetylpenicillamine was not affected. These results indicate that chronic exposure to aluminum impairs glutamate‐induced activation of nitric oxide synthase and nitric oxide‐induced activation of guanylate cyclase. Impairment of the glutamate‐nitric oxide‐cyclic GMP pathway in neurons may contribute to aluminum neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Aluminum Impairs Neuronal Glutamate‐Nitric Oxide‐Cyclic GMP Pathway

Cucarella

Montoliú

Hermenegildo

et al. 1998

Journal of Neurochemistry

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“…However, the accumulation of Al is of no physiological or biological function in mammalian species Chen et al, 2010;Walton, 2012) and can even exert neurotoxicity on organisms (Kumar and Gill, 2009;Poirier et al, 2011;Wu et al, 2012). Humans are more vulnerable to Al toxicity (Gonda and Lehotzky, 1996;Flaten, 2001). Therefore, due to aluminum's wide usage and existence its effects on human health should not be ignored.…”

Section: Introductionmentioning

confidence: 99%

Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

et al. 2013

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-Epidemiological investigations have indicated that aluminum (Al), as an important environmental neurotoxicant, could cause damage to the cognitive function which was closely related with neurodegenerative diseases. Long-term potentiation (LTP) is one form of synaptic plasticity in association with cognitive function. Previous studies have demonstrated that Al impaired early phase long-term potentiation (E-LTP) in vivo and in vitro. However, Al-induced damage to late phase long-term potentiation (L-LTP) has poorly been studied. The present study was designed to observe the effects of subchronic Al exposure on the spatial memory, hippocampus ultrastructure and L-LTP in rats. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation from parturition to weaning for 3 weeks and then fed with the distilled water containing 0, 0.2%, 0.4% and 0.6% aluminum chloride (AlCl 3 ) respectively from weaning to postnatal 3 months. The levels of Al in blood and hippocampus were quantitated by atomic absorption spectrophotometer. Morris water maze test was performed to study spatial memory. The induction and maintenance of L-LTP in area of Schaffer collateral-CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. Hippocampus was collected for transmission electron microscopy observation. The results showed that the Al concentrations in blood and hippocampus of Al-exposed rats were higher than those of the control rats. Al could impair spatial memory ability of rats. Neuronal and synaptic ultrastructure from Al-exposed rats presented pathological changes; the incidence of L-LTP has a decrease trend while population spike (PS) amplitude was much smaller significantly stimulated by high-frequency stimulation (HFS) in Al-exposed rats. Our findings showed that Al exposure caused spatial memory damage, under which the neuronal and synaptic ultrastructure changes maybe were their morphological basis and the impaired L-LTP of hippocampus could be their electrophysiological basis.

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“…Numerous rodent studies have shown that Al exposure during the perinatal period and/or adulthood has deleterious effects on physiological and behavioral development, including loss of body weight, decreased locomotor activity, impaired active avoidance, and decreased spatial memory performance . The doses of Al orally administered to animals in most previous studies seem to be relatively high and are estimated to be a few to more than 10 times higher than the doses given to the mice (0.97‐9.78 mg Al/kg/d) in this study.…”

Section: Discussionmentioning

confidence: 61%

“…Animal studies have been performed to determine whether exposure to Al compounds such as aluminum chloride, aluminum nitrate, and aluminum lactate at different developmental stages affects the brain and behavior. Perinatal and/or adult exposure to Al compounds has been reported to induce behavioral changes such as reduced locomotor activity, impaired active and passive avoidance behaviors, and spatial memory deficits in rodents . In contrast, multiple studies report that Al exposure has no such behavioral effects .…”

Section: Introductionmentioning

confidence: 99%

Behavioral effects of long‐term oral administration of aluminum ammonium sulfate in male and female C57BL/6J mice

Shoji

Irino

Yoshida

et al. 2018

Neuropsychopharm Rep

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Effect of Prenatal Aluminium Lactate Exposure on Conditioned Taste Aversion and Passive Avoidance Task in the Rat

Cited by 21 publications

References 2 publications

Chronic Exposure to Aluminum Impairs Neuronal Glutamate‐Nitric Oxide‐Cyclic GMP Pathway

Chronic Exposure to Aluminum Impairs Neuronal Glutamate‐Nitric Oxide‐Cyclic GMP Pathway

Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

Behavioral effects of long‐term oral administration of aluminum ammonium sulfate in male and female C57BL/6J mice

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