P1‐025: Peripheral administration of lipopolysaccharide induces a deficit in a rodent spatial learning and memory task
Year: 2009
Type: article
Abstract: Chronic inflammation in the central nervous system (CNS) is thought to play a role in spatial learning and memory deficits that are prevalent in neurodegenerative diseases such as Alzheimer's disease (Rosi et al. 2005). Systemic inflammation, with the increase in circulating inflammatory mediators has been shown to trigger a CNS inflammation response (Ru et al. 2005). Hence, the aim of the present study was to determine whether systemic inflammation induced by lipopolysaccharide (LPS) injection is able to elicit cognitive deficits as determined by a rodent spatial learning and memory task. Lister-hooded rats (200-250g, n=10) received increasing doses of LPS over ten days (0.25-16mg/kg; twice daily; 1mL/kg, intraperitoneally). Spatial learning and memory performance was assessed post-treatment using the Morris water maze (2, 4, 6, 8, 12, and 24 weeks). All data was analysed with a repeated-measures ANOVA with planned comparisons. No significant treatment effect was detected in groups rested for 2, 4, or 6 weeks post-treatment. Interestingly, when animals were tested 8 or 12 weeks after LPS treatment, there was a significant increase in latency and path length to locate the submerged platform on spatial cue day 1. However, in animals that were rested for 24 weeks after LPS treatment, no spatial learning deficit was observed. It has been shown that spatial learning and memory involve the preferential recruitment of adult-generated neurons of a certain age in the dentate gyrus (Kee et al. 2007). Hence, these data suggest that the CNS inflammation induced by peripheral LPS administration may disrupt the recruitment of these adult-generated neurons of 8 to 12 weeks of age, thus disrupting the formation of a spatial memory. In conclusion, peripheral LPS administration using the increasing dose regime is able to elicit a robust and reproducible deficit 8 to 12 weeks post-treatment; suggesting that the cognitive deficits observed in chronic neuroinflammatory diseases may be associated with the alteration of neurogenesis processes in the CNS.
Source: Alzheimer s & Dementia
Authors: Fong Kuan K. Wong, Woei Shin S. Chen, Peter Tsun Hon T.H. Wong, Paul Frederick, F. Chapman
Institution: National University of Singapore
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2013414705