Neuronal nitric oxide synthase has a role in the detrimental effects of lipopolysaccharide on spatial memory and synaptic plasticity in rats

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.

Keywords: Lipopolysaccharide; Memory; Neuronal nitric oxide; Synaptic plasticity.