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Inducible Nitric Oxide Inhibitor Aminoguanidine, Ameliorates Deleterious Effects of Lipopolysaccharide on Memory and Long Term Potentiation in Rat Publisher Pubmed



Anaeigoudari A1 ; Soukhtanloo M2 ; Reisi P3 ; Beheshti F4 ; Hosseini M5
Authors
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Authors Affiliations
  1. 1. Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran
  2. 2. Department of Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  3. 3. Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  5. 5. Neurocognitive Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Source: Life Sciences Published:2016


Abstract

Aim An interaction between nitric oxide (NO) and neuro-inflammation has been considered to modulate learning and memory. In the present study, the effect of an inducible NO synthase (iNOS) inhibitor, aminoguanidine (AG) on lipopolysaccharide (LPS)-induced memory impairment was evaluated. Materials and methods The rats were divided and treated: Control (Saline), LPS, AG - LPS and AG, before behavioral and electrophysiological experiments. Results The escape latency in Morris water maze (MWM) test and the latency to enter the dark compartment in Passive avoidance (PA) test in LPS group were significantly higher than in control (P < 0.001) whereas, in AG-LPS group they were shorter than LPS group (P < 0.001). The amplitude and slope of field excitatory post synaptic potential (fEPSP) decreased in LPS group compared to control group (P < 0.05 and P < 0.01) whereas, in AG-LPS group they were higher than LPS group (P < 0.05). Malondialdehyde (MDA) and NO metabolites concentrations in the hippocampus and serum TNFα level of LPS group were higher than control group (P < 0.001, P < 0.05 and 0.01 respectively) while, in AG- LPS group they were lower than LPS group (P < 0.001and P < 0.01 respectively). The thiol content and the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus of LPS group reduced compared to control group (P < 0.001 and P < 0.05 respectively) while, in AG - LPS group they enhanced compared to LPS (P < 0.001 and P < 0.05 respectively). Conclusion It is suggested that increased NO has a role in LPS-induced learning and LTP impairments and the brain tissues oxidative damage which are preventable by iNOS inhibitor aminoguanidine. © 2016
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