Protective effects of lithium treatment for spatial memory deficits induced by tau hyperphosphorylation in splenectomized rats

摘要: 1. Postoperative cognitive dysfunction has become more prevalent in recent years. We used a splenectomized rat model with postoperative spatial learning and memory deficits to investigate the role of tau hyperphosphorylation glycogen synthase kinase-3β (GSK-3β) within hippocampus. 2. Cognitive function was assessed Y-maze 1 day before 1, 3 7 days after surgery. measured site-specific phosphorylation hippocampal (Thr-205 Ser-396), GSK-3β activity expression interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α) mRNA protein as markers inflammation. also tested effects treatment lithium chloride (LiCl), inhibitor. 3. Splenectomy associated impairment later, well rapid massive at Thr-205 Ser-396, activated GSK-3β, increased IL-1β TNF-α expression. LiCl completely restored control levels. 4. These data from suggest that inflammatory factors affect pathology through signalling pathway is promising for deficits.