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Inducing amnesia through systemic suppression

Published version
Peer-reviewed

Type

Article

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Authors

Hulbert, JC 
Henson, RN 
Anderson, MC 

Abstract

Hippocampal damage profoundly disrupts the ability to store new memories of life events. Amnesic windows might also occur in healthy people due to disturbed hippocampal function arising during mental processes that systemically reduce hippocampal activity. Intentionally suppressing memory retrieval (retrieval stopping) reduces hippocampal activity via control mechanisms mediated by the lateral prefrontal cortex. Here we show that when people suppress retrieval given a reminder of an unwanted memory, they are considerably more likely to forget unrelated experiences from periods surrounding suppression. This amnesic shadow follows a dose-response function, becomes more pronounced after practice suppressing retrieval, exhibits characteristics indicating disturbed hippocampal function, and is predicted by reduced hippocampal activity. These findings indicate that stopping retrieval engages a suppression mechanism that broadly compromises hippocampal processes and that hippocampal stabilization processes can be interrupted strategically. Cognitively triggered amnesia constitutes an unrecognized forgetting process that may account for otherwise unexplained memory lapses following trauma.

Description

Keywords

adolescent, adult, amnesia, brain, female, functional neuroimaging, hippocampus, humans, magnetic resonance imaging, male, memory, mental recall, prefrontal cortex, repression, psychology, young adult

Journal Title

Nature Communications

Conference Name

Journal ISSN

2041-1723
2041-1723

Volume Title

7

Publisher

Nature Publishing Group
Sponsorship
MRC (unknown)
Medical Research Council (MC_U105579226)
This work was supported by a Tom Slick Research Award in Consciousness from the Mind Science Foundation to J.C.H. and M.C.A. and grants from the Medical Research Council (MC-A060-5PR00, MC-US A060-5PR10), as well as from the National Science Foundation (0643321 and a Graduate Research Fellowship to J.C.H. (DGE-0751281)).