Work

Swimming exercise attenuates LPS-induced spatial memory deficits associated with IL-17/NF-κB pathway and synaptic dysfunction in developing mice

Year: 2026

Type: article

Abstract: Background Aerobic exercise is known to enhance learning and memory capabilities, whereas inflammation is detrimental to these cognitive functions. This study aimed to investigate the potential of swimming exercise to mitigate spatial memory deficits induced by lipopolysaccharide (LPS) in developing mice. Results Swimming mitigated spatial memory deficits in LPS-treated mice. Transcriptomic analysis indicated that hippocampal gene expression profiles were significantly associated with inflammatory responses, particularly implicating the IL-17/NF-κB signaling pathway. Further investigation using western blotting demonstrated that LPS administration increased the expression of hippocampal inflammatory factors (IL-6 and IL-17) and components of NF-κB p65, while decreasing synaptic proteins (GluA1). In contrast, swimming exercise reduced hippocampal inflammatory factors and NF-κB pathway components and increased synaptic proteins. Additionally, LPS decreased both the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in the CA1 region, as well as the amplitude of evoked excitatory postsynaptic currents (evoked EPSCs) and long-term potentiation (LTP) in the Schaffer collateral-CA1 pathway. Conversely, swimming exercise restored the frequency and amplitude of sEPSCs in the CA1 region and enhanced the amplitude of EPSCs. In conclusion, swimming alleviates LPS-induced spatial memory deficits in juvenile mice, an effect associated with modulation of the IL-17/NF-κB pathway and the enhancement of synaptic activity.

Source: Frontiers in Immunology

DOI: 10.3389/fimmu.2026.1954022