Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring

Maternal sevoflurane exposure during pregnancy is associated with increased risk for behavioral deficits in offspring. Several studies indicated that neurogenesis abnormality may be responsible for the sevoflurane-induced neurotoxicity, but the concrete impact of sevoflurane on fetal brain developme...

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Main Authors: Ruixue Song, Xiaomin Ling, Mengyuan Peng, Zhanggang Xue, Jing Cang, Fang Fang
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2017/6158468
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author Ruixue Song
Xiaomin Ling
Mengyuan Peng
Zhanggang Xue
Jing Cang
Fang Fang
author_facet Ruixue Song
Xiaomin Ling
Mengyuan Peng
Zhanggang Xue
Jing Cang
Fang Fang
author_sort Ruixue Song
collection DOAJ
description Maternal sevoflurane exposure during pregnancy is associated with increased risk for behavioral deficits in offspring. Several studies indicated that neurogenesis abnormality may be responsible for the sevoflurane-induced neurotoxicity, but the concrete impact of sevoflurane on fetal brain development remains poorly understood. We aimed to investigate whether maternal sevoflurane exposure caused learning and memory impairment in offspring through inducing abnormal development of the fetal prefrontal cortex (PFC). Pregnant mice at gestational day 15.5 received 2.5% sevoflurane for 6 h. Learning function of the offspring was evaluated with the Morris water maze test at postnatal day 30. Brain tissues of fetal mice were subjected to immunofluorescence staining to assess differentiation, proliferation, and cell cycle dynamics of the fetal PFC. We found that maternal sevoflurane anesthesia impaired learning ability in offspring through inhibiting deep-layer immature neuron output and neuronal progenitor replication. With the assessment of cell cycle dynamics, we established that these effects were mediated through cell cycle arrest in neural progenitors. Our research has provided insights into the cell cycle-related mechanisms by which maternal sevoflurane exposure can induce neurodevelopmental abnormalities and learning dysfunction and appeals people to consider the neurotoxicity of anesthetics when considering the benefits and risks of nonobstetric surgical procedures.
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institution Kabale University
issn 1687-966X
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language English
publishDate 2017-01-01
publisher Wiley
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series Stem Cells International
spelling doaj-art-a1794776222d4339957172cd20cb1bc12025-02-03T06:07:04ZengWileyStem Cells International1687-966X1687-96782017-01-01201710.1155/2017/61584686158468Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in OffspringRuixue Song0Xiaomin Ling1Mengyuan Peng2Zhanggang Xue3Jing Cang4Fang Fang5Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaDepartment of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaDepartment of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaDepartment of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaDepartment of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaDepartment of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, ChinaMaternal sevoflurane exposure during pregnancy is associated with increased risk for behavioral deficits in offspring. Several studies indicated that neurogenesis abnormality may be responsible for the sevoflurane-induced neurotoxicity, but the concrete impact of sevoflurane on fetal brain development remains poorly understood. We aimed to investigate whether maternal sevoflurane exposure caused learning and memory impairment in offspring through inducing abnormal development of the fetal prefrontal cortex (PFC). Pregnant mice at gestational day 15.5 received 2.5% sevoflurane for 6 h. Learning function of the offspring was evaluated with the Morris water maze test at postnatal day 30. Brain tissues of fetal mice were subjected to immunofluorescence staining to assess differentiation, proliferation, and cell cycle dynamics of the fetal PFC. We found that maternal sevoflurane anesthesia impaired learning ability in offspring through inhibiting deep-layer immature neuron output and neuronal progenitor replication. With the assessment of cell cycle dynamics, we established that these effects were mediated through cell cycle arrest in neural progenitors. Our research has provided insights into the cell cycle-related mechanisms by which maternal sevoflurane exposure can induce neurodevelopmental abnormalities and learning dysfunction and appeals people to consider the neurotoxicity of anesthetics when considering the benefits and risks of nonobstetric surgical procedures.http://dx.doi.org/10.1155/2017/6158468
spellingShingle Ruixue Song
Xiaomin Ling
Mengyuan Peng
Zhanggang Xue
Jing Cang
Fang Fang
Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
Stem Cells International
title Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
title_full Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
title_fullStr Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
title_full_unstemmed Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
title_short Maternal Sevoflurane Exposure Causes Abnormal Development of Fetal Prefrontal Cortex and Induces Cognitive Dysfunction in Offspring
title_sort maternal sevoflurane exposure causes abnormal development of fetal prefrontal cortex and induces cognitive dysfunction in offspring
url http://dx.doi.org/10.1155/2017/6158468
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