不同剂量的七氟醚通过激活ERK通路和合成大鼠海马ARC蛋白来增强学习记忆功能
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Different doses of sevoflurane facilitate and impair learning and memory function through activation of the ERK pathway and synthesis of ARC protein in the rat hippocampus
背景与目的
研究表明七氟烷可增强或减弱成年大鼠的记忆力。然而，这种双向效应的具体机制尚未明确。
方 法
我们用U0126的海马内微量输注来抑制ERK通路的激活。将雄性SD大鼠随机分为4组：假手术组，SEV 0.11％组，SEV 0.3％组，U0126 0.3％组。所有大鼠均接受U0126或生理盐水注射。将大鼠麻醉，麻醉后立即进行避暗（IA）训练。记忆保留潜伏期在24h后观察。在IA训练后45分钟除去海马，以评估ARC表达，突触蛋白1蛋白水平和ERK的磷酸化水平。
结 果
0.11％七氟烷处理导致ERK通路的快速磷酸化，而0.3%七氟烷抑制磷酸化，后者的改变被U0126在海马中的微量输注逆转。 U0126的局部输注消除了0.3％七氟烷引起的记忆障碍和ERK通路的抑制。与0.11％SEV组相比，0.3％SEV组的ARC蛋白和突触蛋白1表达明显上调。
结 论
七氟烷通过ERK信号通路触发突触可塑性相关的细胞骨架蛋白，这种调节作用可能有助于减少其对记忆功能的减弱。
原始文献摘要
Zhu Q L, Luo Y, Xue Q S, et al. Different doses of sevoflurane facilitate and impair learning and memory function through activation of the ERK pathway and synthesis of ARC protein in the rat hippocampus.[J]. Brain Research, 2017.
Background:Sevoflurane has been shown to stimulate or depress memory in adult rats; however, the cellular mechanism of this bidirectional effect has not been fully investigated.
Methods: We used an intra-hippocampal microinfusion of U0126 to suppress ERK activation. Male SD rats were randomly assigned to four groups: Sham, 0.11%SEV, 0.3%SEV and 0.3%+U0126. They received bilateral injections of U0126 or saline. Rats were anesthetized, and Inhibitory Avoidance (IA) training was performed immediately after anesthesia. The memory retention latency was observed 24 h later.In another experiment, the hippocampus was removed 45 min after IA training to assess ARC expression,the synapsin 1 protein levels and the phosphorylation level of ERK.
Results: Treatment with 0.11%SEV led to rapid phosphorylation of ERK, while 0.3%SEV inhibited phosphorylation;the latter change was reversed by the microinfusion of U0126 in the hippocampus. The memory latency result had similar tendencies. The local infusion of U0126 abolished the 0.3%SEV-induced memory impairment and ERK inhibition. Selective upregulations of ARC and synapsin 1 proteins were observed in the 0.3%SEV group compared with the 0.11%SEV group.
Conclusions:The results indicate that different doses of sevoflurane trigger synaptic plasticity-related cytoskeleton proteins through the ERK signaling pathway. This novel modulation by inhalational agents may help to reduce their side-effects on memory function.
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