Indexed on: 23 Oct '20Published on: 23 Oct '20Published in: The International journal of neuroscience
Infection and inflammation are important pathological mechanism underlying neurodegenerative disorders and altered behavioral outcomes including learning and memory deficits. We tested the effect of agmatine in lipopolysaccharides (LPS)-induced learning and memory deficits in mice. Following 7 days of LPS administration animals were subjected to novel object recognition (NOR) test on day 8 and Morris water maze (MWM) test on days 9-13 for the assessment of its effect on learning and memory. Seven of days LPS treatment but not for 1 or 3 days, produced significant deficits in recognition and spatial memory in mice. In LPS pre-treated mice, agmatine treatment on day 8 resulted in the more exploration to the novel object. Agmatine treatment (day 8-12) in mice showed reduction in the escape latency and time spent in the target quadrant (probe trial) in the MWM test. However, co-administration of agmatine with LPS in mice for 7 days showed higher discrimination index in NOR test on Day-8. This co-administration also showed decrease in escape latency as well as time spent in the target quadrant in MWM test on days 9-13 as compared to LPS control group. Therefore, the results of this present study imply the protective and curative effects of agmatine against LPS mediated loss of memory functions in experimental animals. Highlights1. Subchronic but not acute lipopolysaccharides induce memory deficits2. Lipopolysaccharides impairs recognition and spatial memory in mice.3. Agmatine prevents lipopolysaccharides-induced loss of memory.4. Agmatine reverses deficits in learning and memory by lipopolysaccharides.