Electroconvulsive Shock Effects on a Reactivated Memory Trace: Further Examination

Dawson, Ronald G.; McGaugh, James L.

doi:10.1126/science.166.3904.525

Cited by 79 publications

(41 citation statements)

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“…This is highly problematic for a theory which suggests that amnesic agents act to disrupt restabilisation of memory traces, rendering them irreversibly impaired or even erased (Nader, 2003a;Nader & Hardt, 2009 Duvarci & Nader, 2004). In contrast, several studies have not been able to obtain cue-dependent amnesia e ects at all (Biedenkapp & Rudy, 2004;Blaiss & Janak, 2007;Cammarota, Bevilaqua, Medina, & Izquierdo, 2004;Font & Cunningham, 2012;Taubenfeld, Milekic, & Monti, 2001), emulating earlier replication di culties (see paragraph 1.2.7.8.3, Banker et al, 1969;Dawson & McGaugh, 1969;Gold & King, 1972;Jamieson & Albert, 1970;Squire et al, 1976).…”

Section: Cs = Plus/minusmentioning

confidence: 73%

“…R. Miller & Springer, 1973;Riccio & Richardson, 1984). However, some research teams had trouble replicating CDA e ects (e.g., Dawson & McGaugh, 1969) and alternatives to consolidation theory failed to gain traction (Lewis, 1979). Nevertheless, a more recent demonstration of CDA (Nader et al, 2000a) received considerable attention in the neuroscience community, and the debates of the 1960s and 1970s rapidly resurfaced (see Riccio et al, 2006;Sara & Hars, 2006).…”

Section: Summary and Discussion Of Findingsmentioning

confidence: 99%

“…A number of research teams had di culty replicating cue-dependent amnesia e ects (Banker, Hunt, & Pagano, 1969;Dawson & McGaugh, 1969;Gold & King, 1972;Jamieson & Albert, 1970;Squire, Slater, & Chace, 1976) and, unable to identify a reason for the discrepancy in findings, these authors rallied around consolidation theory. Consequently, the initial reports of cue-dependent amnesia had relative little impact on the prevailing zeitgeist (Riccio & Millin, 2003;Sara & Hars, 2006;Squire, 2006).…”

Section: Reinstatement and Renewalmentioning

confidence: 99%

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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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Section: Cs = Plus/minusmentioning

confidence: 73%

Section: Summary and Discussion Of Findingsmentioning

confidence: 99%

Section: Reinstatement and Renewalmentioning

confidence: 99%

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

Hardwicke¹

2017

Preprint

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“…Memory reactivation may, it is suggested, initiate ''re-consolidation.'' Despite previous evidence questioning this suggestion (15,16), there is renewed interest in it (14,17). This issue is important because the idea that a reminder cue initiates re-consolidation of memory for the original training (13,14) clearly conflicts with the extensive evidence that presentation of a reminder cue without reinforcement (e.g., footshock) initiates extinction of responses associated with that cue (1).…”

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confidence: 99%

Retrieval of memory for fear-motivated training initiates extinction requiring protein synthesis in the rat hippocampus

Vianna

Szapiro

McGaugh

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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269

257

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Evidence that protein synthesis inhibitors induce amnesia in a variety of species and learning paradigms indicates that the consolidation of newly acquired information into stable memories requires the synthesis of new proteins. Because extinction of a response also requires acquisition of new information, extinction, like original learning, would be expected to require protein synthesis. The present experiments examined the involvement of protein synthesis in the hippocampus in the extinction of a learned fear-based response known to involve the hippocampus. Rats were trained in a one-trial inhibitory avoidance task in which they received footshock after stepping from a small platform to a grid floor. They were then given daily retention tests without footshock. The inhibitory response (e.g., remaining on the platform) gradually extinguished with repeated testing over several days. Footshock administered in a different context, instead of a retention test, prevented the extinction. Infusions of the protein synthesis inhibitor anisomycin (80 g) into the CA1 region of the hippocampus (bilaterally) 10 min before inhibitory avoidance training impaired retention on all subsequent tests. Anisomycin infused into the hippocampus immediately after the 1st retention test blocked extinction of the response. Infusions administered before the 1st retention test induced a temporary (i.e., 1 day) reduction in retention performance and blocked subsequent extinction. These findings are consistent with other evidence that anisomycin blocks both the consolidation of original learning and extinction.re-consolidation ͉ anisomycin ͉ reminder treatments E xtensive evidence indicates that the extinction of a learned response, like the original learning, requires acquisition of new information (1, 2). During extinction of an aversively based response, for example, a cue formerly associated with a particular consequence (e.g., footshock) becomes associated with a new consequence (e.g., no footshock). The considerable evidence that many drugs have comparable effects on the acquisition and extinction of responses indicates that acquisition and extinction share common mechanisms. Systemic injections of the GABAergic (related to ␥-aminobutyric acid) antagonist picrotoxin enhance retention of many kinds of tasks, including fear-based tasks when administered posttraining (3) and, additionally, enhance extinction of fear conditioning when administered after an extinction session (4). Intrahippocampal administration of the GABAergic agonist muscimol, which impairs consolidation of different forms of contextual fear (5), also impairs context-specific extinction (2). The N-methyl-D-aspartate (NMDA) antagonist APV blocks the consolidation of many tasks (5-8) and also blocks both the consolidation (5) and the extinction of conditioned fear tasks (9). Recent findings indicate that infusions of the protein synthesis inhibitor anisomycin or the ␤-adrenoreceptor antagonist propranolol administered into the insular cortex block both the consolidation (1...

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“…This basic empirical claim was followed by controversy over both its repeatability and generality (e.g., Dawson and McGaugh 1969) and its proper theoretical interpretation: Was the resulting amnesia due to the destruction of the memory trace or did the amnestic agent just render the memory temporarily inaccessible (see Miller and Springer 1973)? Perhaps for these reasons research interest in these phenomena lay dormant until fairly recently.…”

mentioning

confidence: 99%

Anisomycin and the reconsolidation hypothesis

Rudy

Biedenkapp²,

Moineau³

et al. 2006

Learn. Mem.

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Electroconvulsive Shock Effects on a Reactivated Memory Trace: Further Examination

Cited by 79 publications

References 2 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

Retrieval of memory for fear-motivated training initiates extinction requiring protein synthesis in the rat hippocampus

Anisomycin and the reconsolidation hypothesis

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