Repeated Sevoflurane Exposures in Neonatal Rats Increased the Brain Vulnerability to Future Stress Exposure and Resulted in Fear Extinction Deficit.

Tytuł:: Repeated Sevoflurane Exposures in Neonatal Rats Increased the Brain Vulnerability to Future Stress Exposure and Resulted in Fear Extinction Deficit.
Autorzy:: Chen BZ; Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China and Sichuan Provincial Women's and Children's Hospital, Chengdu, China.
Jiang LH; Department of Operating Room Nursing, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Tan L; Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China.
Zhou WQ; Department of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, China.
Shang YC; Department of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, China.
Li F; Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China.
Liu B; Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. .
Źródło:: Neurotoxicity research [Neurotox Res] 2022 Oct; Vol. 40 (5), pp. 1405-1414. Date of Electronic Publication: 2022 Aug 02.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: <2009-> : New York : Springer
Original Publication: [Amsterdam?] : Harwood Academic Publishers,
MeSH Terms:: Anesthetics, Inhalation*/toxicity
Methyl Ethers*/adverse effects
Symporters*
Animals ; Animals, Newborn ; Brain ; Bumetanide/pharmacology ; Cations/pharmacology ; Chlorides ; Extinction, Psychological ; Fear ; Male ; Rats ; Rats, Sprague-Dawley ; Sevoflurane/toxicity ; gamma-Aminobutyric Acid
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Grant Information:: 19ZD009 Key research project of Health Commission of Sichuan Province
Contributed Indexing:: Keywords: Fear extinction; NKCC1/KCC2 ratio; Neonatal sevoflurane; Neuroapoptosis; Stress exposure
Substance Nomenclature:: 0 (Anesthetics, Inhalation)
0 (Cations)
0 (Chlorides)
0 (Methyl Ethers)
0 (Symporters)
0Y2S3XUQ5H (Bumetanide)
38LVP0K73A (Sevoflurane)
56-12-2 (gamma-Aminobutyric Acid)
Entry Date(s):: Date Created: 20220802 Date Completed: 20220929 Latest Revision: 20220929
Update Code:: 20240105
DOI:: 10.1007/s12640-022-00529-z
PMID:: 35917085
: Czasopismo naukowe

Pełny tekst

Sevoflurane anesthesia during neonatal period was reported to sensitize the rodent animals to stress later in life. The authors tested the hypothesis that repeated sevoflurane exposures in neonatal rats increased the brain vulnerability to future stress exposure and resulted in fear extinction deficit and investigated whether the neonatal brain depolarizing γ-aminobutyric acid type A receptor (GABA A R) is involved in mediating these abnormalities. Neonatal Sprague-Dawley male rats, pretreated with vehicle or the NKCC1 inhibitor, bumetanide, received sequential exposures to 3% sevoflurane for 2 h on postnatal days (P) 5, P6, and P7 and then were exposed to electric foot shock stress in fear conditioning training at P14. Juvenile rats at different developmental brain stage receiving identical sevoflurane exposures on P25, P26, and P27 were also studied. The results showed repeated sevoflurane exposures in neonatal rats and increased the cation-chloride cotransporters NKCC1/KCC2 ratio in the PFC at P14. Repeated exposures to sevoflurane in neonatal rather than juvenile rats enhanced the stress response and exacerbated neuroapoptosis in the PFC after exposed to electric foot shock in fear conditioning training. Neonatal rather than juvenile sevoflurane-exposed rats exhibited deficits in fear extinction training and recall. Pretreatment of neonatal rats prior to sevoflurane exposures with bumetanide reduced the NKCC1/KCC2 ratio at P14 and ameliorated most of the subsequent adverse effects. Our study indicates that repeated sevoflurane exposures in neonatal rats might increase the brain vulnerability to future stress exposure and resulted in fear extinction deficit, which might be associated with the neonatal enhanced brain depolarizing GABA A R activity.
(© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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