由异氨酸诱导的神经发生的减少,该神经发生源于三级牙基质
Xin-Li Xiao1, Da-Meng Pan2, Zhe-Qian Zhang3
1Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China; Institute of Neuroscience, Translational Medicine Institute, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Journal of chemical neuroanatomy
|August 18, 2023
概括
麻醉剂的暴露,如异氨酸,会损害年轻小鼠的大脑细胞的发育,影响神经发生并导致认知缺陷. 这种损伤影响到特定的大脑区域,而不是所有,并且与细胞损失和关键的分子通路有关.
科学领域:
- 神经科学是一个神经科学.
- 发展生物学 发展生物学
- 麻醉学 麻醉学
背景情况:
- 麻醉剂可以扰乱发育中的大脑的神经发生,可能导致认知缺陷.
- 动物中的牙状神经发生源于不同的位置:二级矩阵,三级矩阵和亚粒区 (SGZ).
- 麻醉剂对这些个体部位的神经发生的具体影响仍然不清楚.
研究的目的:
- 调查异富对神经发生的作用,其来源于产后的二次牙矩阵,三级牙矩阵和SGZ.
- 确定异类暴露对不同发育阶段细胞增殖,存活和神经元分化的影响.
- 探索麻醉诱导的神经发生障碍的潜在分子机制和行为后果.
主要方法:
- 产后第1,7和31天的小鼠在注射BrdU以标记增殖细胞后暴露于异.
- 定量增殖细胞,不成熟和成熟的颗粒细胞在牙状.
- 通过切割的caspase-3水平和使用NeuN染色的神经元分化来评估细胞损失.
- 利用mRNA测序来识别受影响的分子通路.
- 使用莫里斯水迷宫任务评估认知功能.
主要成果:
- 暴露于异氨酸显著减少了从三级牙状基质和产后二级牙状基质衍生的增殖细胞和不成熟/成熟颗粒细胞,但不是SGZ.
- 观察到的细胞数量的减少主要是由于细胞损失增加而不是神经元分化受损.
- 确定PI3K/Akt/GSK-3β通路对于异氨酸诱导的从三级牙基质中增殖细胞的损失至关重要.
- 在P1和P7小鼠中暴露于异黄素,但不是P31小鼠,导致莫里斯水迷宫任务的缺陷.
结论:
- 异氨酸以特定位置的方式扰乱牙神经发生,主要影响三级牙基质和产后二级牙基质.
- 在生命早期,麻醉诱导的神经发生障碍与PI3K/Akt/GSK-3β通路介导的细胞损失有关.
- 早期接触异黄素会导致持久的认知缺陷,突出显示发育中的大脑对麻醉剂的脆弱性.
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