This preprint is under consideration at Molecular Neurobiology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Research Article
Hongliang Liu
Chongqing University Cancer Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7265-1556
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This work is licensed under a CC BY 4.0 License. Read Full License
Neuroinflammation can cause cognitive deficits, and pre-existing neuroinflammation is very common in the clinic after trauma, surgery, and infection. Patients with pre-existing neuroinflammation often need further medical treatment under general anesthesia. However, it is still unknown the effects of postconditioning with general anesthetics on the pre-existing neuroinflammation. In this study, adult rats were post-treated with sevoflurane or propofol after intracerebroventricular administration of lipopolysaccharide. The effects of sevoflurane or propofol postconditioning on neuroinflammation-induced recognition memory deficit 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 response of general anesthetics. However, postconditioning with propofol induced a selective long-lasting upregulation of extrasynaptic NR2B-containing NMDARs in the dorsal hippocampus, which down-regulated the CREB signaling pathway, and impaired spatial recognition memory. Additionally, the NR2B antagonists, memantine and Ro2506981, reversed this neurotoxicity induced by propofol postconditioning. Altogether, these results indicate that under the pre-existing neuroinflammation, postconditioning with sevoflurane can provide reliable neuroprotection through attenuating LPS-induced neuroinflammation, apoptosis, neuronal loss, and eventually improving spatial recognition deficit. However, although posttreatment with propofol also have the same anti-neuroinflammatory effects, the neurotoxicity caused by propofol postconditioning following neuroinflammation deserves to be continuously concerned.
Keywords
sevoflurane, propofol, neuroinflammation, neuroprotection, neurotoxicity, NMDA receptor
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This preprint is under consideration at Molecular Neurobiology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Hongliang Liu
Chongqing University Cancer Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7265-1556
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 10 Mar, 2021
No community comments so far
Reviewers invited
Invitations sent on 07 Mar, 2021
Editor invited
On 03 Mar, 2021
Editor assigned
On 01 Mar, 2021
First submitted
On 25 Feb, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Neurobiology of Disease
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Neuroinflammation can cause cognitive deficits, and pre-existing neuroinflammation is very common in the clinic after trauma, surgery, and infection. Patients with pre-existing neuroinflammation often need further medical treatment under general anesthesia. However, it is still unknown the effects of postconditioning with general anesthetics on the pre-existing neuroinflammation. In this study, adult rats were post-treated with sevoflurane or propofol after intracerebroventricular administration of lipopolysaccharide. The effects of sevoflurane or propofol postconditioning on neuroinflammation-induced recognition memory deficit 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 response of general anesthetics. However, postconditioning with propofol induced a selective long-lasting upregulation of extrasynaptic NR2B-containing NMDARs in the dorsal hippocampus, which down-regulated the CREB signaling pathway, and impaired spatial recognition memory. Additionally, the NR2B antagonists, memantine and Ro2506981, reversed this neurotoxicity induced by propofol postconditioning. Altogether, these results indicate that under the pre-existing neuroinflammation, postconditioning with sevoflurane can provide reliable neuroprotection through attenuating LPS-induced neuroinflammation, apoptosis, neuronal loss, and eventually improving spatial recognition deficit. However, although posttreatment with propofol also have the same anti-neuroinflammatory effects, the neurotoxicity caused by propofol postconditioning following neuroinflammation deserves to be continuously concerned.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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