Postconditioning with Sevoflurane or Propofol Alleviates Lipopolysaccharide-Induced Neuroinflammation but Exerts Dissimilar Effects on the NR2B Subunit and Cognition
Autor: | Bin Wang, Hongliang Liu, Xiaoyuan Deng, Bianqin Guo, Bo Chen, Xiaoyun Dou |
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Rok vydání: | 2021 |
Předmět: |
Lipopolysaccharides
Male 0301 basic medicine Neuroscience (miscellaneous) Pharmacology Hippocampus Receptors N-Methyl-D-Aspartate Neuroprotection Spatial memory Sevoflurane Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience Cognition 0302 clinical medicine medicine Animals Propofol Neuroinflammation business.industry Memantine Neurotoxicity Recognition Psychology medicine.disease Rats 030104 developmental biology Neurology Neuroinflammatory Diseases NMDA receptor business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Molecular Neurobiology. 58:4251-4267 |
ISSN: | 1559-1182 0893-7648 |
Popis: | 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. |
Databáze: | OpenAIRE |
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