异丙酚麻醉后大鼠海马神经元肌动蛋白重组可能与早期学习记忆障碍有关

Xuena Zhang, Jie Li
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摘要

目的观察异丙酚麻醉后海马肌动蛋白和树突棘的变化,并评价这些变化在幼龄(3月龄)和老年(20月龄)雄性大鼠随后的学习障碍中的作用。方法采用穿梭箱法评价麻醉后1、3、7、14天的学习情况。免疫荧光染色和western blot检测海马CA1区F-actin含量和树突棘。结果老龄大鼠逃避反应潜伏期明显延长至麻醉后7 d,学习曲线发生偏移。老龄大鼠在麻醉后7天内树突棘也减少,F-actin含量显著增加,直至麻醉后14天。结论异丙酚麻醉对大鼠的学习有抑制作用,尤其是对老年大鼠。肌动蛋白的过度聚合和随后海马树突棘的重组可能是导致这种学习障碍的原因。我们的发现提示突触可塑性可能是围手术期神经认知障碍的潜在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Actin reorganization in hippocampal neurons may play a role in early learning and memory impairment after propofol anesthesia in rats
Objectives To observe changes in actin and dendritic spines in the hippocampus after propofol anesthesia, and to evaluate the role of these changes in subsequent learning impairment in both young (3-month-old) and aged (20-month-old) male rats. Methods The shuttle box test was used to evaluate learning from 1, 3, 7, or 14 days after anesthesia. Both F-actin content and dendritic spines in the hippocampal CA1 region were observed using immunofluorescent staining and western blot assays. Results The latency of the escape response was significantly prolonged until 7 days after anesthesia in the aged rats, and their learning curves were shifted. Dendritic spines were also decreased in the aged rats within 7 days after anesthesia, and F-actin content was significantly increased until 14 days after anesthesia. Conclusions Learning was inhibited after propofol anesthesia, especially in aged rats. The over-polymerization of actin and subsequent reorganization of dendritic spines in the hippocampus may be responsible for this learning impairment. Our findings suggest that synaptic plasticity may be an underlying mechanism of perioperative neurocognitive disorders.
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