Isoflurane-induced reduction in neurogenesis derived from the tertiary dentate matrix

IF 2.7 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of chemical neuroanatomy Pub Date : 2023-10-01 DOI:10.1016/j.jchemneu.2023.102325
Xin-Li Xiao , Da-Meng Pan , Zhe-Qian Zhang , Tao Wang , Ding-Hui Li , Chu-Tong Zhang , Le-Fan Liu , Yu Chen , Shu-Nan Yang , Jing Tan , Guan-Ling Fu , Yan-Bing Ma , Xiao-Lin Wu , Jin-Song Zhou , Feng Wu , Kai-Wei Si , Jian-Xin Liu
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Abstract

Anesthetics-induced disruption of dentate neurogenesis in the young brain is strongly suggested to contribute to delayed neurocognitive deficit. In postnatal rodents, the neurogenesis of the dentate gyrus (DG) is sequentially derived from the secondary dentate matrix, tertiary dentate matrix and subgranular zone (SGZ). However, the effects of anesthetics on the dentate neurogenesis derived from specific sites are poorly understood. To trace the new cells generated from the postnatal secondary dentate matrix, peak stage of the tertiary dentate matrix and early stage of the SGZ after isoflurane exposure, mice at postnatal day 1 (P1), P7 and P31 were injected with BrdU at 12 h before the exposure. We found that isoflurane exposure significantly reduced the numbers of proliferating cells (1 day old), immature granule cells (21 days old) or mature granule cells (42 days old) derived from the peak stage of the tertiary dentate matrix and postnatal secondary dentate matrix, but not from the SGZ. Quantitative assessment of BrdU-/BrdU+NeuN-positive cells and cleaved caspase-3 level in the DG indicated that the reduction was correlated with cell loss rather than neuronal differentiation. Mechanistically, we demonstrated that the PI3K/Akt/GSK-3β pathway enriched by mRNA-sequencing is a requirement for the isoflurane-induced loss of 1-day-old proliferating cells generated from the tertiary dentate matrix. In addition, this study demonstrated that P1 and P7 mice, but not P31 mice exposure to isoflurane resulted in subsequent deficits in performance of the tasks of the Morris Water Maze.

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异氟醚诱导的来自第三齿状基质的神经发生减少
麻醉药引起的齿状神经发生在年轻大脑的破坏被强烈建议有助于延迟神经认知缺陷。在出生后的啮齿动物中,齿状回(DG)的神经发生依次来源于二级齿状基质、三级齿状基质和亚颗粒带(SGZ)。然而,麻醉药对源自特定部位的齿状神经发生的影响尚不清楚。为了追踪异氟醚暴露后,小鼠出生后第1天(P1)、P7和P31的小鼠在暴露前12 h注射BrdU,观察其新生细胞的生成情况,以及第三齿状基质的高峰阶段和SGZ的早期阶段。我们发现,异氟醚暴露显著减少了来自第三齿状基质和出生后二级齿状基质高峰阶段的增殖细胞(1日龄)、未成熟颗粒细胞(21日龄)或成熟颗粒细胞(42日龄)的数量,但没有来自SGZ。对DG中BrdU-/BrdU+ neun阳性细胞和cleaved caspase-3水平的定量评估表明,这种降低与细胞损失有关,而与神经元分化无关。从机制上讲,我们证明了通过mrna测序富集的PI3K/Akt/GSK-3β通路是异氟醚诱导的由三级齿状基质产生的1日龄增殖细胞损失的必要条件。此外,本研究表明,暴露于异氟醚的P1和P7小鼠(而非P31小鼠)会导致莫里斯水迷宫任务的后续表现缺陷。
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来源期刊
Journal of chemical neuroanatomy
Journal of chemical neuroanatomy 医学-神经科学
CiteScore
4.50
自引率
3.60%
发文量
87
审稿时长
62 days
期刊介绍: The Journal of Chemical Neuroanatomy publishes scientific reports relating the functional and biochemical aspects of the nervous system with its microanatomical organization. The scope of the journal concentrates on reports which combine microanatomical, biochemical, pharmacological and behavioural approaches. Papers should offer original data correlating the morphology of the nervous system (the brain and spinal cord in particular) with its biochemistry. The Journal of Chemical Neuroanatomy is particularly interested in publishing important studies performed with up-to-date methodology utilizing sensitive chemical microassays, hybridoma technology, immunocytochemistry, in situ hybridization and receptor radioautography, to name a few examples. The Journal of Chemical Neuroanatomy is the natural vehicle for integrated studies utilizing these approaches. The articles will be selected by the editorial board and invited reviewers on the basis of their excellence and potential contribution to this field of neurosciences. Both in vivo and in vitro integrated studies in chemical neuroanatomy are appropriate subjects of interest to the journal. These studies should relate only to vertebrate species with particular emphasis on the mammalian and primate nervous systems.
期刊最新文献
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