Retrieval per se is not sufficient to trigger reconsolidation of human fear memory

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• 作者：Dieuwke Sevenster^a ; ^{d.sevenster@uva.nl} ; Tom Beckers^a ; ^b ; ^{tom.beckers@uva.nl} ; Merel Kindt^a ; ^{m.kindt@uva.nl}
• 关键词：Reconsolidation ; Fear conditioning ; Prediction error ; Plasticity ; Propranolol (尾-blocker) ; Human fear memory
• 刊名：Neurobiology of Learning and Memory
• 出版年：2012
• 期刊代码：81_10747427
• 类别：neu
• 出版时间：March, 2012
• 卷：97
• 期：3
• 页码：338-345
• 文件大小：447 K

摘要

Ample evidence suggests that consolidated memories, upon their retrieval, enter a labile state, in which they might be susceptible to change. It has been proposed that memory labilization allows for the integration of relevant information in the established memory trace (memory updating). Memory labilization and reconsolidation do not necessarily occur when a memory is being reactivated, but only when there is something to be learned during memory retrieval (prediction error). Thus, updating of a fear memory trace should not occur under retrieval conditions in which the outcome is fully predictable (no prediction error). Here, we addressed this issue, using a human differential fear conditioning procedure, by eliminating the very possibility of reinforcement of the reminder cue. A previously established fear memory (picture-shock pairings) was reactivated with shock-electrodes attached (Propranolol group, n = 18) or unattached (Propranolol No-Shock Expectation group, n = 19). We additionally tested a placebo-control group with the shock-electrodes attached (Placebo group, n = 18). Reconsolidation was not triggered when nothing could be learned during the reminder trial, as noradrenergic blockade did not affect expression of the fear memory 24 h later in the Propranolol No-Shock Expectation group. Only when the outcome of the retrieval cue was not fully predictable, propranolol, contrary to placebo, reduced the startle fear response and prevented the return of fear (reinstatement) the following day. In line with previous studies, skin conductance response and shock expectancies were not affected by propranolol. Remarkably, a double dissociation emerged between the emotional (startle response) and more cognitive expression (expectancies, SCR) of the fear memory. Our findings have important implications for reconsolidation blockade as treatment strategy for emotional disorders. First, fear reducing procedures that target the emotional component of fear memory do not necessarily affect the cognitive component and vice versa. Second, mere retrieval of the fear memory is not sufficient to induce its labilization and reconsolidation.