Prereactivation propranolol fails to reduce skin conductance reactivity to prepared fear‐conditioned stimuli

Spring, Justin D.; Wood, N.; Mueller‐Pfeiffer, Christoph; Milad, Mohammed R.; Pitman, Roger K.; Orr, Scott P.

doi:10.1111/psyp.12326

Cited by 36 publications

(45 citation statements)

References 49 publications

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“…Interventions are often delivered before the reminder in studies using propranolol (which are not included in the systematic aspect of this review; e.g., Kindt et al, 2009;Schwabe, Nader, & Pruessner, 2013;Spring et al, 2015;Soeter & Kindt, 2010 because the drug typically takes around 90m to reach peak plasma concentration in the blood (Schiller & Phelps, 2011).…”

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confidence: 99%

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

Hardwicke¹

2017

Preprint

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The human memory system must resolve a critical tension, ensuring that knowledge endures over time (persistence), whilst simultaneously retaining a capacity for updating when knowledge is outdated or erroneous (plasticity). In this thesis, I examine the provocative idea that memory traces can be overwritten with new information, especially during transient periods of retrieval-induced plasticity that occur when a trace undergoes reconsolidation. A systematic review of human reconsolidation studies finds that the evidentiary support for this claim is remarkably tenuous. Furthermore, the theory fails to survive several strong empirical tests. In Experiments 1-7, I do not replicate a previous finding that is widely cited as a convincing demonstration of human reconsolidation. In Experiments 8-10, I revisit the ‘destructive updating’ account of the classic ‘misinformation effect’ in the context of reconsolidation theory. These experiments show that the effect can be eliminated when an appropriate recognition test is used, demonstrating that event traces are not irrecoverably lost, and therefore cannot have been overwritten during reconsolidation. In Experiment 11, I examine whether prior retrieval will help or hinder the correction of naturally occurring semantic misconceptions. Contrary to reconsolidation theory, I find that knowledge updating is not contingent on memory retrieval, nor does it result in the overwriting of prior knowledge.Finally, in the context of media ‘breaking news’ reports (Experiment 12), I find that the provision of an explicit retraction message, coupled with an alternative account with high causal coverage, is insufficient to eliminate reliance on false information. Finally, I contend that the widespread proliferation of ad hoc hypotheses, and the absence of systematic direct replication, has caused the field of reconsolidation to descend into a theoretical quagmire.I make several recommendations based on the principles of open science that may help to restore mechanisms of self-correction and foster genuine theoretical progress.

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confidence: 99%

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

Hardwicke¹

2017

Preprint

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“…Failure to reduce fear to the reactivated and non-reactivated CS+s in the present study may be due, at least in part, to the combined use of prepared, fear-relevant stimuli and selection of subjects who demonstrated strong SCR conditionability and reported a predisposition to being afraid of spiders. As noted in Spring et al (2015), it is possible that in our efforts to produce differential conditioning that would be more resistant to a floor effect we actually produced conditioning that was highly resistant to intervention. The strength of the conditioned SCR to the reactivated CS+ may have been so strong that a single exposure to the CS+R, unpaired with the US, was simply inadequate to produce reconsolidation blockade.…”

Section: Discussionmentioning

confidence: 99%

“…As observed by Spring et al (2015), the differential conditioning procedure, combined with setting a differential conditioning threshold for SCRs, produced robust responses to the stimuli that would subsequently serve as the reactivated (CS+R) and non-reactivated (CS+N) cues, by which reconsolidation blockade of conditioned fear responses was assessed. Differential SCRs to the CS+R and CS+N, compared to their respective CS-presentations, remained largely intact and significant across subsequent testing of renewal and reinstatement on day 3) and reacquisition (4-weeks).…”

Section: Discussionmentioning

confidence: 99%

“…Reconsolidation blockade was tested on the following day (day 3) by examining spontaneous recovery and reinstatement of the conditioned SCR. In an attempt to establish fear-conditioned SCRs that are more resistant to extinction and that might serve to test the relative strengths of various drug and non-drug candidates for reconsolidation blockade, we employed more highly prepared CSs, more fear-sensitive subjects, and stronger conditioned responses (CRs), as done previously by Spring et al (2015). It has been shown that certain classes of CSs, when paired with a US, produce a stronger fear CR, i.e., they are more "prepared" to enter into an association with the US (Mineka & Öhman, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…This procedure was previously used to test the whether or not propranolol could reduce reconsolidation of a fear-conditioned skin conductance response (SCR; Spring et al, 2015). Spring et al found that the differential conditioning procedure, combined with setting a differential conditioning threshold for acquired SCRs, produced robust responses to the stimuli that could subsequently serve as suitable conditioned stimuli to be reactivated (CS+R) or not (CS+N), by which reconsolidation blockade of conditioned fear responses could be assessed.…”

Section: Mifepristone Reduces Skin Conductance Reactivity To Fear-conmentioning

confidence: 99%

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Psychophysiology of Delayed Extinction and Reconsolidation in Humans

Orr¹

2015

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) AND ADDRESS(ES) PERFORMING ORGANIZATION REPORT NUMBERMassachusetts General Hospital Boston, Massachusetts 02114 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S)U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTAnimal research suggests that reactivation (retrieval) of a consolidated memory can return it to a labile state from which it must be restabilized in order to persist. This stabilization process has been termed "reconsolidation", and various behavioral and pharmacological interventions have been found to modify or block it. The aim of this project was to create an experimental assay in the form of an optimal Pavlovian differential fear-conditioning paradigm, within which the relative strengths of various pharmacological and behavioral, reconsolidation-blocking interventions could be tested. We completed testing for two pharmacological interventions and a behavioral intervention. Study of a third pharmacological intervention was initiated.Results from propranolol and behavioral intervention groups demonstrated differential conditioning learning on Day 1, supporting the validity of our modified fear-conditioning paradigm. Propranolol administration and the behavioral intervention at the time of memory reactivation did not decrease the fear memory, as indexed by skin conductance, when assessing renewal and reinstatement. Mifepristone was tested as a second pharmacological intervention. After adjusting for initial differences in conditioned response strength, results suggest that mifepristone did reduce the fear memory. Results from a third pharmacological intervention, oxytocin, tentatively suggest a generalized reduction of the fear memory. SUBJECT TERMSPost-traumatic stress disorder; reconsolidation; fear conditioning; psychophysiology

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Threat processing: models and mechanisms

Bentz

Schiller

2015

WIRES Cognitive Science

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The experience of fear is closely linked to the survival of species. Fear can be conceptualized as a brain state that orchestrates defense reactions to threats. To avoid harm, an organism must be equipped with neural circuits that allow learning, detecting, and rapidly responding to threats. Past experience with threat can transform neutral stimuli present at the time of experience into learned threat-related stimuli via associative learning. Pavlovian threat conditioning is the central experimental paradigm to study associative learning. Once learned, these stimulus-response associations are not always expressed depending on context or new experiences with the conditioned stimuli. Neural circuits mediating threat learning have the inherent plasticity to adapt to changing environmental threats. Encounters devoid of danger pave the way for extinction or reconsolidation to occur. Extinction and reconsolidation can both lead to changes in the expression of threat-induced defense responses, but differ in stability and have a different neural basis. This review presents the behavioral models and the system-level neural mechanisms in animals and humans of threat learning and modulation.

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Prereactivation propranolol fails to reduce skin conductance reactivity to prepared fear‐conditioned stimuli

Cited by 36 publications

References 49 publications

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

Persistence and plasticity in the human memory system: An empirical investigation of the overwriting hypothesis

Psychophysiology of Delayed Extinction and Reconsolidation in Humans

Threat processing: models and mechanisms

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