Inducible nitric oxide inhibitor aminoguanidine, ameliorates deleterious effects of lipopolysaccharide on memory and long term potentiation in rat

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 TNF alpha 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 < 0.001 and 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. (C) 2016 Elsevier Inc. All rights reserved.