Internalization of GluA2 and the underlying mechanisms of cognitive decline in aged rats following surgery and prolonged exposure to sevoflurane.

摘要: Abstract Background We revealed that a high concentration of sevoflurane exacerbated cognitive impairment in aged rats, and the inhibition GluA2 subunit internalization facilitated neuroprotection after cerebral ischemic injury. However, trafficking POCD its underlying mechanism are not clear. thus detected effects for different inhalation durations on postoperative function investigated role this process. Methods A rat model orthopedic surgery was performed with 1.5 MAC inhalation. Cognitive evaluated by manipulating Y maze fear conditioning tests 7 days experiments. Western blot, ELISA coimmunoprecipitation were applied to analyze internalization, PI3K expression activity, as well alterations MEF2-Arc pathway hippocampus. Neuron apoptosis spine morphology hippocampus also observed. Results found neuron increased following 2 h, possibly due decrease PI3K-GluA2 complex activity prolonged observed contributed long-term function, which impaired spinal 2 h. Conclusion The above results suggest 2 h potentiated surgery-impaired PI3K-AMPAR activation signal contributes stages POCD.