Zanghi Christine N, Jevtovic-Todorovic Vesna
University of Colorado, Anschutz Medical Campus, Department of Anesthesiology, 12801 E. 17th Ave., Mail Stop 8130, Aurora, CO 80045, United States.
Neurotoxicol Teratol. 2017 Mar-Apr;60:24-32. doi: 10.1016/j.ntt.2016.12.004. Epub 2016 Dec 28.
The year 2016 marked the 15th anniversary since anesthesia-induced developmental neurotoxicity and its resulting cognitive dysfunction were first described. Since that time, multiple scientific studies have supported these original findings and investigated possible mechanisms behind anesthesia-induced neurotoxicity. This paper reviews the existing mechanistic literature on anesthesia-induced neurotoxicity in the context of a holistic approach that emphasizes the importance of both neuronal and non-neuronal cells during early postnatal development. Sections are divided into key stages in early neural development; apoptosis, neurogenesis, migration, differentiation, synaptogenesis, gliogenesis, myelination and blood brain barrier/cerebrovasculature. In addition, the authors combine the established literature in the field of anesthesia-induced neurotoxicity with literature from other related scientific fields to speculate on the potential role of non-neuronal cells and to generate new future hypotheses for understanding anesthetic toxicity and its application to the practice of pediatric anesthesia.
2016年是麻醉诱导发育神经毒性及其所致认知功能障碍首次被描述后的第15个年头。自那时起，多项科学研究支持了这些最初的发现，并对麻醉诱导神经毒性背后的可能机制进行了研究。本文在一种整体方法的背景下，回顾了关于麻醉诱导神经毒性的现有机制文献，该方法强调了出生后早期发育过程中神经元和非神经元细胞的重要性。章节分为早期神经发育的关键阶段；细胞凋亡、神经发生、迁移、分化、突触形成、神经胶质生成、髓鞘形成以及血脑屏障/脑血管系统。此外，作者将麻醉诱导神经毒性领域的既有文献与其他相关科学领域的文献相结合，推测非神经元细胞的潜在作用，并为理解麻醉毒性及其在小儿麻醉实践中的应用提出新的未来假设。
