Neonatal exposure to sevoflurane caused cognitive deficits by dysregulating SK2 channels and GluA2-lacking AMPA receptors in juvenile rat hippocampus

Yu, Xiangyou; Zhang, Fangxiang; Shi, Jing‐Shan

doi:10.1016/j.neuropharm.2018.08.014

Cited by 28 publications

(24 citation statements)

References 38 publications

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“…BDNF increases the number of inhibitory and excitatory synapses, promotes synapse formation, participates in LTP, and is related to learning and memory ( 17 ). LTP is the neuronal basis of learning and memory ( 18 ), and the MWM is a classical and reliable method to evaluate spatial learning and memory in animal models ( 19 – 21 ). In the present study, we found that when rats were exposed to 2.5% sevoflurane for 3 h during late pregnancy, no differences in the expression of Ac-H3, Ac-H4, HDAC2, HDAC3, or BDNF were observed in their offspring at P35.…”

Section: Discussionmentioning

confidence: 99%

Enriched environment improves sevoflurane-induced cognitive impairment during late-pregnancy via hippocampal histone acetylation

Yu¹,

Zhang²,

Wang³

et al. 2020

Braz J Med Biol Res

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Fetal exposure to sevoflurane induces long-term cognitive impairment. Histone acetylation regulates the transcription of genes involved in memory formation. We investigated whether sevoflurane exposure during late-pregnancy induces neurocognitive impairment in offspring, and if this is related to histone acetylation dysfunction. We determined whether the effects could be reversed by an enriched environment (EE). Pregnant rats were exposed to 2.5% sevoflurane or control for 1, 3, or 6 h on gestational day 18 (G18). Sevoflurane reduced brain-derived neurotrophic factor (BDNF), acetyl histone H3 (Ac-H3), and Ac-H4 levels and increased histone deacetylases-2 (HDAC2) and HDAC3 levels in the hippocampus of the offspring on postnatal day 1 (P1) and P35. Long-term potentiation was inhibited, and spatial learning and memory were impaired in the 6-h sevoflurane group at P35. EE alleviated sevoflurane-induced cognitive dysfunction and increased hippocampal BDNF, Ac-H3, and Ac-H4. Exposure to 2.5% sevoflurane for 3 h during late-pregnancy decreased hippocampal BDNF, Ac-H3, and Ac-H4 in the offspring but had no effect on cognitive function. However, when the exposure time was 6 h, impaired spatial learning and memory were linked to reduced BDNF, Ac-H3, and Ac-H4, which could be reversed by EE.

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Section: Discussionmentioning

confidence: 99%

Enriched environment improves sevoflurane-induced cognitive impairment during late-pregnancy via hippocampal histone acetylation

Yu¹,

Zhang²,

Wang³

et al. 2020

Braz J Med Biol Res

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“…Morris water maze test was performed to assess spatial learning and memory of rats treated with ketamine and genistein according to previous studies (Li et al., 2014; Yu, Zhang, & Shi, 2018). Briefly, experimental rats were subjected to a 5‐day training session starting from P60 followed by a probe trial on the 6th day.…”

Section: Methodsmentioning

confidence: 99%

Genistein attenuates cognitive deficits and neuroapoptosis in hippocampus induced by ketamine exposure in neonatal rats

Zhang

2020

Synapse

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Ketamine is a frequently used anesthetic in pediatric patients that can cause cognitive impairment. Genistein, a bioactive component of soy products, has been shown to suppress neuronal death through regulating the expression of apoptosis related genes. In this study, we hypothesized that genistein could alleviate ketamine‐induced cognitive impairment by ameliorating hippocampal neuronal loss and tested this hypothesis in rats. Neonatal rats were treated with ketamine and genistein. Hippocampal tissue was harvested for histological and biochemical analysis to determine neuronal apoptosis and proteins involved in the apoptotic pathways. Behavioral assays including contextual fear conditioning test and Morris water maze test were performed to assess cognitive functions, including learning and memory. We found that in fear conditioning test, genistein restored freezing time in ketamine treated rats in a dose dependent manner. Similarly, genistein attenuated impaired learning and memory in Morris water maze test in rats treated with ketamine. Additionally, ketamine‐induced neuronal apoptosis in rat hippocampus was attenuated by genistein treatment. Finally, we found that genistein partially restored proteins associated with apoptosis, including Bax, Bcl‐2, cleaved caspase 3, and phosphorylated GSK‐3ß and Akt. Genistein suppresses hippocampal neuronal loss and cognitive disruption induced by ketamine in rats.

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“…Sevoflurane exposure. Rats in the control group were untreated, and those in the two sevoflurane exposure groups (S1 and S2) were exposed to 2% sevoflurane (15)(16)(17)(18). All rats were placed in separate cages and treated using 100% oxygen as a carrier gas, with a 4 l/min total gas flow.…”

Section: Animalsmentioning

confidence: 99%

Effects of sevoflurane general anesthesia during early pregnancy on AIM2 expression in the hippocampus and parietal cortex of Sprague‑Dawley offspring rats

Zhu

Liu

et al. 2021

Exp Ther Med

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The aim of the present study was to investigate the effect of exposure to sevoflurane general anesthesia during early pregnancy on interferon-inducible protein AIM2 (AIM2) expression in the hippocampus and parietal cortex of the offspring Sprague-Dawley (SD) rats. A total of 18 SD rats at a gestational age of 5-7 days were randomly divided into three groups: i) A control group (control); ii) 2-h sevoflurane general anesthesia, group 1 (S1); and iii) 4-h sevoflurane general anesthesia, group 2 (S2). The six offspring rats in each group were maintained for 30 days and assessed by Morris water maze testing. Brain specimens were collected from offspring rats 30 days after birth. Changes in the structural morphology of neurons in the hippocampus and parietal cortex were observed using hematoxylin and eosin staining. Nissl bodies in the hippocampus and parietal cortex were observed by Nissl staining. The expression of glial fibrillary acidic protein (GFAP), AIM2, CD45 and IL-1β was detected by immunohistochemistry and the protein levels of CD45, IL-1β, pro-caspase-1 and caspase-1 p10 were detected by western blotting. Compared with the control group, offspring rats in the S1 and S2 groups exhibited poor long-term learning and memory ability and experienced different degrees of damage to both the hippocampus and parietal cortex. The expression levels of GFAP, AIM2, CD45, IL-1β, caspase-1 and caspase-1 p10 in the offspring of both the S1 and the S2 groups were significantly increased (P<0.05) compared with offspring of the control group. Moreover, compared with the offspring of the S1 group, hippocampal and parietal cortex injury in the offspring of the S2 group was further aggravated, and the expression of GFAP, AIM2, CD45, IL-1β, pro-caspase-1 and cleaved-caspase-1 was significantly increased (P<0.05). In conclusion, sevoflurane general anesthesia in SD rat early pregnancy promoted the expression of AIM2 and the inflammatory response in the hippocampus and parietal cortex of offspring rats.

show abstract

Neonatal exposure to sevoflurane caused cognitive deficits by dysregulating SK2 channels and GluA2-lacking AMPA receptors in juvenile rat hippocampus

Cited by 28 publications

References 38 publications

Enriched environment improves sevoflurane-induced cognitive impairment during late-pregnancy via hippocampal histone acetylation

Enriched environment improves sevoflurane-induced cognitive impairment during late-pregnancy via hippocampal histone acetylation

Genistein attenuates cognitive deficits and neuroapoptosis in hippocampus induced by ketamine exposure in neonatal rats

Effects of sevoflurane general anesthesia during early pregnancy on AIM2 expression in the hippocampus and parietal cortex of Sprague‑Dawley offspring rats

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