Preventing and treating PTSD-like memory by trauma contextualization

被引：32

作者：

Al Abed, Alice Shaam ^{[1
,2
,3
]}

Ducourneau, Eva-Gunnel ^{[1
,2
]}

Bouarab, Chloe ^{[1
,2
,4
]}

Sellami, Azza ^{[1
,2
]}

Marighetto, Aline ^{[1
,2
]}

Desmedt, Aline ^{[1
,2
]}

机构：

[1] INSERM, U1215, Neuroctr Magendie Physiopathol Plast Neuronale, F-33000 Bordeaux, France

[2] Univ Bordeaux, F-33000 Bordeaux, France

[3] Australian Natl Univ, John Curtin Sch Med Res, Eccles Inst Neurosci, Canberra, ACT, Australia

[4] George Washington Univ, Ross Hall Room 7272,300 Eye I St NW, Washington, DC 20037 USA

来源：

NATURE COMMUNICATIONS | 2020年 / 11卷 / 01期

关键词：

POSTTRAUMATIC-STRESS-DISORDER; MECHANISMS; BRAIN; CONSOLIDATION; MODULATION; AMYGDALA; CA1; MRI;

D O I：

10.1038/s41467-020-18002-w

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Post-traumatic stress disorder (PTSD) is characterized by emotional hypermnesia on which preclinical studies focus so far. While this hypermnesia relates to salient traumatic cues, partial amnesia for the traumatic context can also be observed. Here, we show in mice that contextual amnesia is causally involved in PTSD-like memory formation, and that treating the amnesia by re-exposure to all trauma-related cues cures PTSD-like hypermnesia. These findings open a therapeutic perspective based on trauma contextualization and the underlying hippocampal mechanisms. Individuals with PTSD are unable to recollect contextual cues related to the trauma. Here the authors show that this contextual amnesia, associated with the inhibition of hippocampal activity, is causally involved in PTSD-like hypermnesia in mice, and that re-exposure to all trauma-related cues eliminates PTSD-like memory while promoting normal fear memory.

引用

页数：9

共 32 条

[1] Adult neurogenesis: From precursors to network and physiology [J].