期刊
MOLECULAR NEUROBIOLOGY
卷 -, 期 -, 页码 -出版社
SPRINGER
DOI: 10.1007/s12035-021-02402-0
关键词
Sevoflurane; Propofol; Neuroinflammation; Neuroprotection; Neurotoxicity; NMDA receptor
资金
- National Science Foundation Project of Chongqing [cstc2017jcyjBX0043, cstc2019jcyj-msxmX0608]
The study found that postconditioning with sevoflurane could reverse the cognitive deficits induced by neuroinflammation and provide reliable neuroprotection. On the other hand, postconditioning with propofol, while also anti-neuroinflammatory like sevoflurane, caused neurotoxicity leading to impairments in spatial recognition memory.
Neuroinflammation can cause cognitive deficits, and preexisting neuroinflammation is observed frequently in the clinic after trauma, surgery, and infection. Patients with preexisting neuroinflammation often need further medical treatment under general anesthesia. However, the effects of postconditioning with general anesthetics on preexisting neuroinflammation have not been determined. In this study, adult rats were posttreated with sevoflurane or propofol after intracerebroventricular administration of lipopolysaccharide. The effects of sevoflurane or propofol postconditioning on neuroinflammation-induced recognition memory deficits were detected. Our results found that postconditioning with sevoflurane but not propofol reversed the selective spatial recognition memory impairment induced by neuroinflammation, and these differential effects did not appear to be associated with the similar anti-neuroinflammatory responses of general anesthetics. However, postconditioning with propofol induced a selective long-lasting upregulation of extrasynaptic NR2B-containing N-methyl-D-aspartate receptors in the dorsal hippocampus, which downregulated the cAMP response element-binding signaling pathway and impaired spatial recognition memory. Additionally, the NR2B antagonists memantine and Ro25-6981 reversed this neurotoxicity induced by propofol postconditioning. Taken together, these results indicate that under preexisting neuroinflammation, postconditioning with sevoflurane can provide reliable neuroprotection by attenuating lipopolysaccharide-induced neuroinflammation, apoptosis, and neuronal loss and eventually improving spatial recognition deficits. However, although posttreatment with propofol also has the same anti-neuroinflammatory effects, the neurotoxicity caused by propofol postconditioning following neuroinflammation warrants further consideration.
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