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Potentiating Role of Copper on Spatial Memory Deficit Induced by Beta Amyloid and Evaluation of Mitochondrial Function Markers in the Hippocampus of Rats Publisher Pubmed



Behzadfar L1 ; Abdollahi M1 ; Sabzevari O1 ; Hosseini R1 ; Salimi A2 ; Naserzadeh P3 ; Sharifzadeh M1 ; Pourahmad J3
Authors
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Authors Affiliations
  1. 1. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, P.O. Box 14155-6451, Tehran, Iran
  2. 2. Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Science, Ardabil, Iran
  3. 3. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, P.O. Box 14155, Tehran, 6153, Iran

Source: Metallomics Published:2017


Abstract

Mounting evidence suggests that copper, a crucial element in normal brain function, plays an important role in the etiology of Alzheimer's disease, which is known as a neurodegenerative mitochondrial disorder. However, the precise mechanisms of its effects on cognitive and mitochondrial functions through the CNS have not been thoroughly recognized yet. In this study, we aimed to investigate the long-term (3-week) effects of copper sulfate (50, 100 and 200 mg kg-1 day-1) exposure on learning and memory as well as on mitochondrial function in the hippocampus of rats in the presence and absence of beta amyloid (1 μg μl-1 per side) intrahippocampally (IH). After three weeks of copper exposure through drinking water, acquisition and retention of spatial memory were measured by the Morris water maze (MWM) test. Various parameters of mitochondrial function were also evaluated. Our data show that copper damaged the spatial learning and memory and also exacerbated the memory deficit induced by Aβ injection in rats in a dose-dependent manner. Mitochondria isolated from the hippocampus of rats treated with copper showed significant increases in ROS formation, mitochondrial swelling, lipid peroxidation, glutathione oxidation, outer membrane damage, and collapse of MMP, decreased cytochrome c oxidase activity, and finally increased ADP/ATP ratios. Our results indicate that copper overloading in the hippocampus of rats causes mitochondrial dysfunction and subsequent oxidative stress leading to cognitive impairment. This study also reveals that copper can potentiate Aβ deleterious effects on spatial memory and brain mitochondrial function. © 2017 The Royal Society of Chemistry.
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