Rombold F, Wingenfeld K, Renneberg B, Hellmann-Regen J, Otte C, Roepke S
Department of Psychiatry and Psychotherapy,Charité - Universitätsmedizin Berlin,Campus Benjamin Franklin,Berlin,Germany.
Department of Psychology,Freie Universitaet Berlin,Berlin,Germany.
Psychol Med. 2016 Sep;46(12):2523-34. doi: 10.1017/S0033291716001379. Epub 2016 Jun 23.
Intrusive memories of traumatic events are a core feature of post-traumatic stress disorder but little is known about the neurobiological formation of intrusions. The aim of this study was to determine whether the activity of the noradrenergic system during an intrusion-inducing stressor would influence subsequent intrusive memories.
We conducted an experimental, double-blind, placebo-controlled study in 118 healthy women. Participants received a single dose of either 10 mg yohimbine, stimulating noradrenergic activity, or 0.15 mg clonidine, inhibiting noradrenergic activity, or placebo. Subsequently, they watched an established trauma film which induced intrusions. The number of consecutive intrusions resulting from the trauma film, the vividness of the intrusions, and the degree of distress evoked by the intrusions were assessed during the following 4 days. Salivary cortisol and α-amylase were collected before and after the trauma film.
A significant time × treatment interaction for the number of intrusions and the vividness of intrusions indicated a different time course of intrusions depending on treatment. Post-hoc tests revealed a delayed decrease of intrusions and a delayed decrease of intrusion vividness after the trauma film in the yohimbine group compared with the clonidine and placebo groups. Furthermore, after yohimbine administration, a significant increase in salivary cortisol levels was observed during the trauma film.
Our findings indicate that pharmacological activation of the noradrenergic system during an emotionally negative event makes an impact on consecutive intrusive memories and their vividness in healthy women. The noradrenergic system seems to be involved in the formation of intrusive memories.
创伤事件的侵入性记忆是创伤后应激障碍的核心特征，但对于侵入性记忆的神经生物学形成知之甚少。本研究的目的是确定在诱发侵入性记忆的应激源期间去甲肾上腺素能系统的活动是否会影响随后的侵入性记忆。
我们对118名健康女性进行了一项实验性、双盲、安慰剂对照研究。参与者接受单剂量的10毫克育亨宾（刺激去甲肾上腺素能活动）、0.15毫克可乐定（抑制去甲肾上腺素能活动）或安慰剂。随后，她们观看一部既定的创伤影片，该影片会诱发侵入性记忆。在接下来的4天里，评估创伤影片引发的连续侵入性记忆的数量、侵入性记忆的生动程度以及侵入性记忆所引发的痛苦程度。在观看创伤影片前后收集唾液皮质醇和α-淀粉酶。
侵入性记忆数量和侵入性记忆生动程度的显著时间×治疗交互作用表明，根据治疗方法的不同，侵入性记忆的时间进程也不同。事后检验显示，与可乐定组和安慰剂组相比，育亨宾组在观看创伤影片后侵入性记忆数量的下降延迟，侵入性记忆生动程度的下降也延迟。此外，在给予育亨宾后，观看创伤影片期间观察到唾液皮质醇水平显著升高。
我们的研究结果表明，在情绪负面事件期间对去甲肾上腺素能系统进行药理学激活会对健康女性随后的侵入性记忆及其生动程度产生影响。去甲肾上腺素能系统似乎参与了侵入性记忆的形成。
