Hippocampus is more vulnerable to neural damages induced by repeated sevoflurane exposure in the second trimester than other brain areas.
hippocampus
m6A
sevoflurane
vulnerability
Journal
Acta biochimica et biophysica Sinica
ISSN: 1745-7270
Titre abrégé: Acta Biochim Biophys Sin (Shanghai)
Pays: China
ID NLM: 101206716
Informations de publication
Date de publication:
05 Aug 2020
05 Aug 2020
Historique:
received:
23
12
2019
pubmed:
10
6
2020
medline:
7
1
2021
entrez:
10
6
2020
Statut:
ppublish
Résumé
During the rapidly developing and sensitive period of the central nervous system (CNS), a harmful stimulus may have serious consequences. The effect of anesthetic exposure on the development of the offspring's CNS during pregnancy is still unclear and has been widely concerned. In the present study, we compared the susceptibility of the hippocampus with those of other brain regions in offsprings when the mother mice were exposed to repeated sevoflurane. We found that other than affecting motor sensation, emotion, or social behavior of offspring mice, repeated sevoflurane exposure induced significant memory deficiency. Compared with other brain regions, the hippocampus, which is the key component of the brain serving for learning and memory, was more vulnerable to repeated sevoflurane exposure. We also found that repeated sevoflurane exposure to mother mice could inhibit the axon development of hippocampal neurons. We also predicted that N6-methyladenosine modification of mRNA might play an essential role in the vulnerability of the hippocampus to sevoflurane, while the underlying cellular mechanism needs to be explored in the future. Our study may provide a new perspective for studying the mechanism of hippocampus-specific injury induced by sevoflurane exposure.
Identifiants
pubmed: 32515467
pii: 5854955
doi: 10.1093/abbs/gmaa060
doi:
Substances chimiques
Sevoflurane
38LVP0K73A
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
864-874Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.