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首页> 外文期刊>Frontiers in Neuroscience >Corrigendum: Memory Reinforcement and Attenuation by Activating the Human Locus Coeruleus via Transcutaneous Vagus Nerve Stimulation
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Corrigendum: Memory Reinforcement and Attenuation by Activating the Human Locus Coeruleus via Transcutaneous Vagus Nerve Stimulation

机译：勘误：通过经皮迷走神经刺激激活人轨迹蓝斑，从而增强记忆力和减弱

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In the original article, there was an error. The stimulation intensity and the atVNS effects on anxiety extinction, were incorrectly stated. A correction has been made to the section Locus Coeruleus Activation via Transcutaneous Vagus Nerve Stimulation , subsection Facilitation of Learning Fear Extinction and the Attenuation of Fear Learning : “Neuronal assemblies between the amygdala, hippocampus, anterior cingulated cortex, and ventromedial prefrontal cortex are important for consolidating and extinguishing fear memory (Fullana et al., 2018 ; Marek and Sah, 2018 ). A neuronal correlate of posttraumatic stress disorder (PTSD) is impaired fear-memory extinction. Noradrenaline plays a major role in the pathogenesis of PTSD (Hendrickson and Raskind, 2016 ). AtVNS via LC activation might strengthen the impaired LC-dependent noradrenergic transmission in PTSD modulating fear-memory extinction. Experimental animal evidence suggests that extinction-memory impairment in rats with PTSD-like behavior is reversible by applying iVNS. In addition, PTSD-like behavior in rats (e.g., hyperarousal) can be attenuated by iVNS (Noble et al., 2017 ). However, to date, the atVNS effect on extinction memory has only been investigated in healthy subjects. Extinction memory can be facilitated in healthy subjects, as two recent studies showed (Burger et al., 2016 , 2017 ). Similar concha cymba-atVNS parameters were utilized in both studies (25 Hz, ≤ 0.5 mA) (Burger et al., 2016 , 2017 ), and fear-extinction learning in healthy students was facilitated (Burger et al., 2016 ) (Figure 1). However, the storage of extinction memory one day later was unaffected by atVNS (Burger et al., 2016 ). Another working group demonstrated no atVNS-dependent modulation of anxiety extinction (Genheimer et al., 2017 ) being likely based on various stimulation parameter such as mean intensity (1.2 mA) (Genheimer et al., 2017 ) and timing of atVNS. Overall, these studies reveal promising potential for atVNS as a tool for modulating extinction memory in anxiety disorders”. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
机译：在原始文章中，有一个错误。错误地指出了刺激强度和atVNS对焦虑消退的影响。对通过经皮迷走神经刺激引起的蓝斑蓝斑激活，对学习恐惧消退的促进和对恐惧学习的减弱的小节进行了更正：“杏仁核，海马，前扣带皮层和腹侧前额叶皮层之间的神经元组装对于巩固和消除恐惧记忆（Fullana et al。，2018; Marek and Sah，2018）。创伤后应激障碍（PTSD）的神经元相关联的恐惧记忆消失。去甲肾上腺素在PTSD的发病机理中起主要作用（Hendrickson and Raskind，2016）。通过LC激活的AtVNS可能会增强PTSD调节恐惧记忆消退中受损的依赖LC的去甲肾上腺素能传递。动物实验证据表明，通过应用iVNS，具有PTSD样行为的大鼠的记忆消失是可以逆转的。此外，iVNS可以减轻大鼠PTSD样的行为（例如，高度兴奋）（Noble等人，2017年）。然而，迄今为止，仅在健康受试者中研究了atVNS对灭绝记忆的作用。正如两项最新研究表明的那样，在健康受试者中可以促进灭绝记忆（Burger等人，2016，2017）。两项研究（25 Hz，≤0.5 mA）使用了相似的外耳c（cocha cymba-atVNS）参数（Burger等人，2016，2017），并促进了健康学生的恐惧消灭学习（Burger等人，2016）（图1）。但是，一天后灭绝记忆的存储不受atVNS的影响（Burger等，2016）。另一个工作组表明，不可能基于多种刺激参数（如平均强度（1.2 mA）（Genheimer等，2017）和atVNS的时间安排）来确定atVNS依赖的对焦虑的消灭（Genheimer等，2017）。总体而言，这些研究显示出atVNS作为调节焦虑症灭绝记忆的工具的潜力很大。作者对此错误表示歉意，并声明这不会以任何方式改变本文的科学结论。原始文章已更新。

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