Loss of dendritic connectivity in CA1, CA2, and CA3 neurons in hippocampus in rat under aluminum toxicity: Antidotal effect of pyridoxine

Sreekumaran, E; Ramakrishna, T.; Madhav, T.R.; Anandh, D; Prabhu, Badanavalu M.; Sulekha, Sindu; Bindu, PS; Raju, T.R.

doi:10.1016/s0361-9230(02)00944-9

Cited by 22 publications

(9 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Results of the AlCl 3 -received group were also confirmed by the results of the histopathological examination of the brain in the present study which showed degeneration and pyknosis in hippocampus neurons, focal gliosis as well as focal eosinophilic plagues in the striatum in addition to congestion in blood vessels. Aluminium toxicity is also associated with reduced axonal length and dendritic branches in hippocampus [48].…”

Section: Discussionmentioning

confidence: 99%

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

View full text Add to dashboard Cite

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized clinically by cognitive decline and memory loss. Caffeine and nicotine are the most commonly co-used psycho stimulants. Caffeine is one of the major contributors to the dietary antioxidants which prevent oxidative damage and may reduce the risk of chronic neurodegenerative diseases. Nicotine has the ability to decrease level of reactive oxygen species (ROS) in the hippocampus and suggested to attenuate the impairment of memory associated with AD. The study aimed to evaluate the influence of caffeine and nicotine co-administration against aluminium-induced neurotoxicity that mimics AD in rats. Five groups of rats were used and received daily for five weeks: Saline for control, aluminium chloride (AlCl 3 ) (70 mg/kg, IP) for AD mimic group, while treated groups received together with AlCl 3 , either Caffeine (5mg/kg, IP), Nicotine (1 mg/kg, SC) or their combination. Three behavioral experiments were performed: Forced Swimming Test (FST), Morris Water Maze (MWM) task and Conditioned-Avoidance and Learning (CAL) test. Histo pathological changes in the brain and biochemical changes in Acetyl cholinesterase (AchE) as well as oxidative parameters; malon dialdehyde (MDA), superoxide dismutase (SOD), total anti oxidane capacity (TAC) were also evaluated for all groups. Results of the behavioral tests showed that caffeine and nicotine co-administration had more pronounced protecting effect from learning and memory impairment induced by AlCl 3 than each one alone. Caffeine and nicotine co-administration also prevent neuronal degeneration in the hippocampus and the eosinophilic plagues in the striatum induced by AlCl 3 while nicotine alone still showed mild gliosis in striatum. The marked protection of caffeine and nicotine co-administration confirmed also by the significant increase in TAC and SOD and decrease in MDA and AchE in brain tissue. In conclusion, co-administration of caffeine and nicotine can reduce the risk of neuronal degeneration in the hippocampus and attenuate the impairment of learning and memory associated with AD.

show abstract

Section: Discussionmentioning

confidence: 99%

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

View full text Add to dashboard Cite

show abstract

“…In both brain areas, atrophy and neuron apoptosis were seen to be accompanied by neurofibrillary degeneration, argyrophilic inclusion, Schwann cell degeneration, and nerve fibre demyelination. Similarly, histopathological examinations of the hippocampus in 2 rat models following Al treatment showed marked changes in general brain histology, as indicated by an increased number of vacuolated spaces [45], and more specifically, effects on the neuronal connectivity in the hippocampus [46]. …”

Section: Discussionmentioning

confidence: 99%

Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks

et al. 2012

View full text Add to dashboard Cite

SummaryBackgroundAluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain.Material/MethodsWe used a chick embryonic development model, with Al treatment of 500 μg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool.ResultsThis Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model.ConclusionsExposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

show abstract

“…When intraperitoneally injected with ecologic doses of aluminum gluconate three times a week for 6 months, adult rats showed behavioral and neuropathological modifications that were observed in AD 16 . When AlCl 3 was injected into the cerebrospinal fluid through the cisterna magna, adult rats showed toxicity which apparently affected neuronal connectivity in the hippocampus, 32 and severe anterograde degeneration of cholinergic terminals in the cortex and hippocampus due to damage of the cingulated bundle 33 although no major signs of gross histological changes were evident in cresyl violet‐stained sections 33 …”

Section: Discussionmentioning

confidence: 99%

“…31 When intraperitoneally injected with ecologic doses of aluminum gluconate three times a week for 6 months, adult rats showed behavioral and neuropathological modifications that were observed in AD. 16 When AlCl 3 was injected into the cerebrospinal fluid through the cisterna magna, adult rats showed toxicity which apparently affected neuronal connectivity in the hippocampus, 32 and severe anterograde degeneration of cholinergic terminals in the cortex and hippocampus due to damage of the cingulated bundle 33 although no major signs of gross histological changes were evident in cresyl violet-stained sections. 33 Although further studies are needed to elucidate the reasons for which sAb1-42 aggregates with AlCl 3 disappear from the rat ventricular system and our short-term coinfusion model of sAb1-42 aggregates with AlCl 3 show no major histopathological findings characteristic of AD, exposure time to aluminum, infused dose or concentration of aluminum, time until sacrifice, species of Ab, age of rats or infusion site may be critical to produce an animal model for AD induced by aluminum toxicity.…”

Section: Discussionmentioning

confidence: 99%

Aluminum chloride does not facilitate deposition of human synthetic amyloid β1–42 peptide in the rat ventricular system of a short‐term infusion model

et al. 2005

View full text Add to dashboard Cite

Recent data have demonstrated that a 39-43 amino acid peptide called beta-amyloid peptide (Abeta), which predominantly contains 42 residues (Abeta1-42), has a strong tendency to form insoluble aggregates and that the toxic effects of Abeta are based on its aggregation. In a previous study, we reported that infusion of 100 microg of human synthetic Abeta1-42 (sAbeta1-42), which is a main component of diffuse plaques, into the lateral ventricle of the rat brain of a short-term infusion model resulted in almost complete disappearance of sAbeta1-42 aggregates from the ventricles by 28 days. In addition, aluminum is considered a potential etiological factor in Alzheimer's disease (AD). Neurotoxicity from excess brain exposure to aluminum has been documented from both clinical observations and animal experiments, although a direct relationship between aluminum and AD has yet to be clearly established. We therefore investigated the effects of sAbeta1-42 aggregates with aluminum chloride (AlCl3) in the ventricular system of the rat brain of a short-term infusion model. At either 2 or 7 days following infusion, sAbeta1-42 formed aggregates with AlCl3 that spread throughout the entire ventricular system. However, sAbeta1-42 aggregates with AlCl3 had almost disappeared from the ventricles by 28 days, resulting in similarities with respect to the time-course and the neuropathological changes observed in sAbeta1-42 aggregation without AlCl3. We herein report for the first time that considerable amounts of sAbeta1-42 aggregates with AlCl3 almost disappear from the rat ventricular system by 28 days post-infusion.

show abstract

Loss of dendritic connectivity in CA1, CA2, and CA3 neurons in hippocampus in rat under aluminum toxicity: Antidotal effect of pyridoxine

Cited by 22 publications

References 23 publications

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks

Aluminum chloride does not facilitate deposition of human synthetic amyloid β1–42 peptide in the rat ventricular system of a short‐term infusion model

Contact Info

Product

Resources

About