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Impaired Memory and Evidence of Histopathology in Ca1 Pyramidal Neurons Through Injection of Aβ1-42 Peptides Into the Frontal Cortices of Rat



Eslamizade MJ1, 3 ; Madjd Z4 ; Rasoolijazi H5 ; Saffarzadeh F1, 3 ; Pirhajati V2 ; Aligholi H3 ; Janahmadi M6 ; Mehdizadeh M2
Authors
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Authors Affiliations
  1. 1. Department of Neuroscience, School of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Shefa Neuroscience Research Center, Khatam Al-anbia Hospital, Tehran, Iran
  4. 4. Department of Pathology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Basic and Clinical Neuroscience Published:2016

Abstract

Introduction: Alzheimer's disease (AD) is one of the most common neurodegenerative disorders, which has much benefited from animal models to find the basics of its pathophysiology. In our previous work (Haghani, Shabani, Javan, Motamedi, & Janahmadi, 2012), a non-transgenic rat model of AD was used in electrophysiological studies. However, we did not investigate the histological aspects in the mentioned study. Methods: An AD model was developed through bilateral injection of amyloid-β peptides (Aβ) into the frontal cortices. Behavioral and histological methods were used to assess alterations in the memory and (ultra)structures. Furthermore, melatonin has been administered to assess its efficacy on this AD model. Results: Passive avoidance showed a progressive decline in the memory following Aβ injection. Furthermore, Nissl staining showed that Aβ neurotoxicity caused shrinkage of the CA1 pyramidal neurons. Neurodegeneration was clearly evident from Fluoro-jade labeled neurons in Aβ treated rats. Moreover, higher NF-κB immunoreactive CA1 pyramidal neurons were remarkably observed in Aβ treated rats. Ultrastructural analysis using electron microscopy also showed the evidence of subcellular abnormalities. Melatonin treatment in this model of AD prevented Aβ- induced increased NF-κB from immunoreaction and neurodegeneration. Discussion: This study suggests that injection of Aβ into the frontal cortices results in the memory decline and histochemical disturbances in CA1 pyramidal neurons. Furthermore, melatonin can prevent several histological changes induced by Aβ.