Fleischer Juliane, Metz Sophie, Düsenberg Moritz, Grimm Simone, Golde Sabrina, Roepke Stefan, Renneberg Babette, Wolf Oliver T, Otte Christian, Wingenfeld Katja
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Klinik für Psychiatrie und Psychotherapie, Campus Benjamin Franklin, Berlin, Germany.
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Klinik für Psychiatrie und Psychotherapie, Campus Benjamin Franklin, Berlin, Germany; MSB Medical School Berlin, Berlin, Germany; Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric Hospital, University of Zurich, Switzerland.
Behav Brain Res. 2019 Feb 1;359:895-902. doi: 10.1016/j.bbr.2018.06.024. Epub 2018 Jun 22.
It is well known that elevated cortisol after stress or after exogenous administration impairs episodic memory retrieval including autobiographical memory (AM) retrieval. This impairment might be mediated by deactivation of a neural network associated with memory retrieval including the prefrontal cortex (PFC) and limbic structures. However, the neural underpinnings of these cortisol effects on AM retrieval have not been investigated yet. In this study, thirty-three healthy women received either placebo or 10 mg hydrocortisone in a double blind cross-over design before completing an AM test during fMRI. In this test, participants are asked to recall specific events from their own past in response to a cue word. In a first step, we analyzed the neural underpinnings of AM retrieval in the placebo condition. We found an activation pattern consistent with core regions involved in autobiographical memory recall, including the ventromedial PFC, anterior medial (am)PFC, inferior frontal gyrus, the posterior cingulate cortex, the tempoparietal junction, the middle temporal gyrus and the hippocampus. Further, we analyzed brain activation during AM retrieval after hydrocortisone compared to placebo. Region of interest (ROI) analyses revealed a hydrocortisone-induced deactivation during AM retrieval in the right amPFC. Results of the ROI analyses were non-significant in the left and right hippocampus, the left and right vmPFC and the left amPFC In sum, during AM retrieval hydrocortisone had the most pronounced effects on the amPFC. This might be explained by the strong involvement of this brain region in self-referential behavior, which is essential for recalling autobiographic information.
众所周知,应激后或外源性给药后皮质醇升高会损害情景记忆提取,包括自传体记忆(AM)提取。这种损害可能是由与记忆提取相关的神经网络失活介导的,该神经网络包括前额叶皮质(PFC)和边缘结构。然而,这些皮质醇对AM提取影响的神经基础尚未得到研究。在本研究中,33名健康女性在功能磁共振成像(fMRI)期间完成AM测试之前,采用双盲交叉设计接受了安慰剂或10毫克氢化可的松。在该测试中,参与者被要求根据提示词回忆自己过去的特定事件。第一步,我们分析了安慰剂条件下AM提取的神经基础。我们发现了一种与自传体记忆回忆所涉及的核心区域一致的激活模式,包括腹内侧前额叶皮质、前内侧前额叶皮质、额下回、后扣带回皮质、颞顶联合区、颞中回和海马体。此外,我们分析了氢化可的松给药后与安慰剂相比AM提取过程中的脑激活情况。感兴趣区域(ROI)分析显示,氢化可的松会导致右侧前内侧前额叶皮质在AM提取过程中失活。ROI分析结果在左右海马体、左右腹内侧前额叶皮质和左侧前内侧前额叶皮质中无显著差异。总之,在AM提取过程中,氢化可的松对前内侧前额叶皮质的影响最为明显。这可能是由于该脑区强烈参与自我参照行为,而自我参照行为对于回忆自传体信息至关重要。