Akbar Anaeigoudari1, Mohammad Soukhtanloo2, Mohammad Naser Shafei3, Hamid Reza Sadeghnia4, Parham Reisi5, Farimah Beheshti1, Sepehr Behradnia3, Seyed Mojtaba Mousavi3, Mahmoud Hosseini6. 1. Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 2. Department of Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 4. Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 5. Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. 6. Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: hosseinim@mums.ac.ir.
Abstract
BACKGROUND: The role of neuronal nitric oxide synthase (nNOS) in lipopolysaccharide (LPS)-induced memory and synaptic plasticity impairment was investigated. METHODS: The rats were divided and treated as follows: (1) control (saline), (2) LPS, (3) 7NI (7-nitroindazole as a nNOS inhibitor)-LPS and (4) 7NI. RESULTS: In a Morris water maze, the LPS group took a longer amount of time and traveled a greater distance to reach the platform, this was prevented by 7NI. Malondialdehyde (MDA) and nitric oxide (NO) metabolites in the hippocampus of the LPS group were higher while the total thiol, superoxide dismutase and catalase were lower than that of the controlled specimen. Pre-treatment using 7NI prevented the changes in the biochemical criteria. The slope and amplitude of the field excitatory post-synaptic potential (fEPSP) in the LPS group decreased, whereas in 7NI-LPS group they increased. CONCLUSION: It is suggested that inhibition of nNOS by 7NI improves the deleterious effects of LPS by reducing NO metabolites and the brain tissues oxidative damage.
BACKGROUND: The role of neuronal nitric oxide synthase (nNOS) in lipopolysaccharide (LPS)-induced memory and synaptic plasticity impairment was investigated. METHODS: The rats were divided and treated as follows: (1) control (saline), (2) LPS, (3) 7NI (7-nitroindazole as a nNOS inhibitor)-LPS and (4) 7NI. RESULTS: In a Morris water maze, the LPS group took a longer amount of time and traveled a greater distance to reach the platform, this was prevented by 7NI. Malondialdehyde (MDA) and nitric oxide (NO) metabolites in the hippocampus of the LPS group were higher while the total thiol, superoxide dismutase and catalase were lower than that of the controlled specimen. Pre-treatment using 7NI prevented the changes in the biochemical criteria. The slope and amplitude of the field excitatory post-synaptic potential (fEPSP) in the LPS group decreased, whereas in 7NI-LPS group they increased. CONCLUSION: It is suggested that inhibition of nNOS by 7NI improves the deleterious effects of LPS by reducing NO metabolites and the brain tissues oxidative damage.
Authors: Sara Memarpour; Farimah Beheshti; Yousef Baghcheghi; Abbas Ali Vafaei; Mahmoud Hosseini; Ali Rashidy-Pour Journal: Neurochem Res Date: 2020-09-15 Impact factor: 3.996