The Role of Histone Acetylation in the Sevoflurane-induced Inhibition of Neurogenesis in the Hippocampi of Young Mice

Jia, Junke; Zhu, Jun; Yang, Qin; Wang, Yanlin; Zhang, Zongze; Chen, Chang

doi:10.1016/j.neuroscience.2020.02.023

Cited by 15 publications

(11 citation statements)

References 50 publications

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“…All 3 Trk receptors were markedly reduced when the SEVO concentration increased to ≥4%. These results are in line with a previous study showing that TrkB was reduced in the hippocampus of SEVO-treated young mice [32]. However, our data, for the first time, provide evidence that SEVO downregulates Trk gene expression in human lineage neuronal cells.…”

Section: Discussionsupporting

confidence: 93%

TrkC Overexpression Protects Sevoflurane-Induced Neurotoxicity in Human Induced Pluripotent Stem Cell-Derived Neurons

et al. 2020

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Background: Inhaled anesthetic sevoflurane (SEVO) may induce cortical neurotoxicity and memory dysfunction in both animals and humans. In this study, we investigated the toxic effects of SEVO on human induced pluripotent stem cell (iPS)-derived neurons. Methods: Human iPS-derived neurons were exposed to SEVO in vitro. SEVO-induced toxic effects were examined with the viability, live caspase 3/7, and neurite density assays, respectively. The effects of SEVO on the receptors of the tyrosine kinases TrkA, TrkB, and TrkC were assessed by qRT-PCR. TrkA, TrkB, and TrkC were ectopically overexpressed in human iPS-derived neurons. Their functional effects on SEVO-induced human iPS-derived neuron toxicity were further investigated. Results: SEVO induced dose-dependent cell death, caspase 3/7 elevation, neurite degeneration, and the downregulation of Trk receptors in human iPS-derived neurons. Adenovirus-mediated Trk receptor overexpression selectively upregulated endogenous TrkA, TrkB, or TrkC gene expressions in human iPS-derived neurons. Specifically, TrkC overexpression, but not TrkA or TrkB overexpression was found to overcome the neurotoxic effects of SEVO in human iPS-derived neurons. Conclusions: SEVO may induce neurotoxicity in human iPS-derived neurons, and its neurotoxic damage could be protected by the overexpression of TrkC.

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Section: Discussionsupporting

confidence: 93%

TrkC Overexpression Protects Sevoflurane-Induced Neurotoxicity in Human Induced Pluripotent Stem Cell-Derived Neurons

et al. 2020

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“…Previous studies have proved that sevoflurane has adverse effects on developing brain such as fetal mice, newborn mice or young mice (Fang et al, 2012;Shen et al, 2013;Wang et al, 2019;Jia et al, 2020). It has been confirmed that sevoflurane exposure of developing brain tend to suffer cognitive impairment in adulthood such as learning and memory deficiency (Shen et al, 2013;Yu et al, 2020).…”

Section: Discussionmentioning

confidence: 91%

“…Kuhn et al (1996) first quantified age-related decline in AHN in old rats through BrdU labeling and IHC analysis. It has been reported that sevoflurane has a dual effect on neurogenesis in young mice (Chen et al, 2015(Chen et al, , 2018Jia et al, 2020). However, there is lack of research to evaluate the effect of sevoflurane on AHN in adult or aged subjects.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Adult Hippocampal Neurogenesis Plays a Role in Sevoflurane-Induced Cognitive Impairment in Aged Mice Through Brain-Derived Neurotrophic Factor/Tyrosine Receptor Kinase B and Neurotrophin-3/Tropomyosin Receptor Kinase C Pathways

Guo

Wang

et al. 2022

Front. Aging Neurosci.

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Sevoflurane anesthesia induces cognitive impairment, which may lead to perioperative neurocognitive disorders (PND). However, the factors and molecular mechanism underlying this impairment remains unclear. Adult hippocampal neurogenesis (AHN) in the subgranular zone of the hippocampus has been implicated in cognitive processes. Nonetheless, the direct role of AHN in sevoflurane-induced cognitive impairment has never been demonstrated. In this study, we explored the age and the concentration factors and the role of AHN inhibition in sevoflurane-induced cognitive impairment in sevoflurane inhalation model mice. We found that 3% sevoflurane exposure induced significant cognitive impairment and inhibition of AHN in aged mice but not adult mice. Expression of BDNF/TrkB and NT-3/TrkC was also decreased by 3% sevoflurane exposure in aged mice. Hippocampal brain-derived neurotrophic factor (BDNF) or Neurotrophin-3 (NT-3) microinjection could partially improve the sevoflurane-induced cognitive impairment and AHN inhibition, respectively. These results demonstrate that the cognitive impairment caused by sevoflurane inhalation is related to patient age and sevoflurane concentration. In conclusion, the molecular mechanism of cognitive impairment in the elderly is related to the inhibition of AHN through the BDNF/TrkB and NT-3/TrkC pathways. Thus, sevoflurane inhalation anesthesia may be safe for adult patients, but caution should be exercised when administering it to the elderly.

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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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The Role of Histone Acetylation in the Sevoflurane-induced Inhibition of Neurogenesis in the Hippocampi of Young Mice

Cited by 15 publications

References 50 publications

TrkC Overexpression Protects Sevoflurane-Induced Neurotoxicity in Human Induced Pluripotent Stem Cell-Derived Neurons

TrkC Overexpression Protects Sevoflurane-Induced Neurotoxicity in Human Induced Pluripotent Stem Cell-Derived Neurons

Inhibition of Adult Hippocampal Neurogenesis Plays a Role in Sevoflurane-Induced Cognitive Impairment in Aged Mice Through Brain-Derived Neurotrophic Factor/Tyrosine Receptor Kinase B and Neurotrophin-3/Tropomyosin Receptor Kinase C Pathways

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

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