Multiple sevoflurane exposures during pregnancy inhibit neuronal migration by upregulating prostaglandin D2 synthase

Chai, Dongdong; Cheng, Yanyong; Sun, Yinghao; Jia, Yan; Hu, Rong; Zhang, Lei; Jiang, Hong

doi:10.1016/j.ijdevneu.2019.09.001

Cited by 10 publications

(6 citation statements)

References 38 publications

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“…Ptgds was known as a prostaglandin D synthase in brain that catalyzed the conversion of prostaglandin H2 to prostaglandin D2, which acted as a neuromodulator and/or trophic factor in the central nervous system ( 54 ). A previous study reported that multiple exposures of sevoflurane-induced neuronal migration deficit in embryonic neocortex were due to the elevated Ptgds expression level ( 55 ), which also supported our results to a certain extent. Here, we preliminarily identified the role of Ptgds in regulating NSC/IPC migration.…”

Section: Discussionsupporting

confidence: 92%

Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms

Sun

You

et al. 2022

Sci. Adv.

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The involvement of genetic risk and the underlying developmental and neural circuit mechanisms in autism-related social deficit are largely unclear. Here, we report that deletion of AUTS2 , a high-susceptibility gene of ASDs, caused postnatal dentate gyrus (DG) hypoplasia, which was closely relevant to social recognition deficit. Furthermore, a previously unknown mechanism for neural cell migration in postnatal DG development was identified, in which Auts2-related signaling played a vital role as the transcription repressor. Moreover, the supramammillary nucleus (SuM)–DG-CA3 neural circuit was found to be involved in social recognition and affected in Auts2 -deleted mice due to DG hypoplasia. Correction of DG-CA3 synaptic transmission by using a pharmacological approach or chemo/optogenetic activation of the SuM-DG circuit restored the social recognition deficit in Auts2 -deleted mice. Our findings demonstrated the vital role of Auts2 in postnatal DG development, and this role was critical for SuM-DG-CA3 neural circuit-mediated social recognition behavior.

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Section: Discussionsupporting

confidence: 92%

Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms

Sun

You

et al. 2022

Sci. Adv.

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“…In addition to its traditionally accepted protective effect by decreasing neuronal death and promoting long-term memory consolidation 26 , an appropriate dose of SPC may facilitate endogenous hippocampal neural network reconstruction through neurogenesis and promotion of migration of astrocytes and microglia to the infarcted region for neurocognitive repairment 27,28 . Moreover, Chai reported that multiple use and overdose of sevoflurane in the pregnant period may directly inhibit neural migration in the cortex of offspring 29 . In our present study, we first investigated DG neuron migration and neuron organization after HIE.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Postconditioning Ameliorates Neuronal Migration Disorder Through Reelin/Dab1 and Improves Long-term Cognition in Neonatal Rats After Hypoxic-Ischemic Injury

Zhang

Gao

et al. 2021

Neurotox Res

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Sevoflurane postconditioning (SPC) had been reported to attenuate developing brain injury after hypoxia-ischemia encephalopathy (HIE)via inhibiting neural necrosis and autophagy process. Moreover, recent report elucidated sevoflurane may involve in neural cells migration after injury. Here we hypothesize neuronal migration and long-term cognition were ruined after HIE and SPC alleviated these injuries .Classical Rice-Vannucci model of Hypoxia-ischemia was conducted on P7 pups , which was followed by SPC at the 1 minimum alveolar concentration (MAC 2.4%) for 30 min. Piceatannol which can cleave Reelin into proteolytic fragments was used to detect whether Reelin/Dab1 is involved in neuroprotection exerted by SPC. Our findings suggest that hypoxia-ischemia disrupted cytoarchitecture of dentate gyrus (DG) by inhibiting the migration of dentate neurons of hippocampus, which may eventually lead to long-term cognition deficits. However, SPC could relieve the restricted hippocampal neurons from the subgranular zone of hippocampi combined with the repair of hippocampal-dependent memory function damaged by HIE through attenuating the overactivation of the Reelin/Dab1pathway. Taken together, these results demonstrate that SPC plays a pivotal role in ameliorating neuronal migration disorder and maintain normal cytoarchitecture and spatial learning ability of DG by regulating the Reelin/Dab1 downstream signaling pathway. This indicates the potential therapeutic use of SPC in treating HIE perinatally.

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“…In contrast, other studies have shown completely different subsets of genes to be altered following anesthetic exposure [33,34,[36][37][38][39][40]. However, in these studies, neither the developmental stages nor the exposure conditions were considered for a fair comparison [33,34,[36][37][38][39][40], thus making these findings inconclusive. Other studies using different anesthetics such as isoflurane [41][42][43][44], propofol [34,43] or ketamine [43,45] have also failed to provide a consensus for specific genes altered by anesthetic exposure, as neither the models used nor the experimental conditions were kept consistent.…”

Section: Introductionmentioning

confidence: 92%

“…For instance, two different studies have claimed that early exposure to sevoflurane in rats, either once [31] or three times [32], results in the downregulation of Krüppel-like factor 4 (Kfl4), a transcription factor involved in cell growth, proliferation, or differentiation [35], over both a shorter [31] and a longer term [32]. In contrast, other studies have shown completely different subsets of genes to be altered following anesthetic exposure [33,34,[36][37][38][39][40]. However, in these studies, neither the developmental stages nor the exposure conditions were considered for a fair comparison [33,34,[36][37][38][39][40], thus making these findings inconclusive.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Exposure in Neonates Perturbs the Expression Patterns of Specific Genes That May Underly the Observed Learning and Memory Deficits

Jimenez-Tellez

Pehar

Visser

et al. 2023

IJMS

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Exposure to commonly used anesthetics leads to neurotoxic effects in animal models—ranging from cell death to learning and memory deficits. These neurotoxic effects invoke a variety of molecular pathways, exerting either immediate or long-term effects at the cellular and behavioural levels. However, little is known about the gene expression changes following early neonatal exposure to these anesthetic agents. We report here on the effects of sevoflurane, a commonly used inhalational anesthetic, on learning and memory and identify a key set of genes that may likely be involved in the observed behavioural deficits. Specifically, we demonstrate that sevoflurane exposure in postnatal day 7 (P7) rat pups results in subtle, but distinct, memory deficits in the adult animals that have not been reported previously. Interestingly, when given intraperitoneally, pre-treatment with dexmedetomidine (DEX) could only prevent sevoflurane-induced anxiety in open field testing. To identify genes that may have been altered in the neonatal rats after sevoflurane and DEX exposure, specifically those impacting cellular viability, learning, and memory, we conducted an extensive Nanostring study examining over 770 genes. We found differential changes in the gene expression levels after exposure to both agents. A number of the perturbed genes found in this study have previously been implicated in synaptic transmission, plasticity, neurogenesis, apoptosis, myelination, and learning and memory. Our data thus demonstrate that subtle, albeit long-term, changes observed in an adult animal’s learning and memory after neonatal anesthetic exposure may likely involve perturbation of specific gene expression patterns.

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Multiple sevoflurane exposures during pregnancy inhibit neuronal migration by upregulating prostaglandin D2 synthase

Cited by 10 publications

References 38 publications

Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms

Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms

Sevoflurane Postconditioning Ameliorates Neuronal Migration Disorder Through Reelin/Dab1 and Improves Long-term Cognition in Neonatal Rats After Hypoxic-Ischemic Injury

Sevoflurane Exposure in Neonates Perturbs the Expression Patterns of Specific Genes That May Underly the Observed Learning and Memory Deficits

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