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      Opposing Mechanisms Support the Voluntary Forgetting of Unwanted Memories

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      1 , , 1
      Neuron
      Cell Press

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          Summary

          Reminders of the past can trigger the recollection of events that one would rather forget. Here, using fMRI, we demonstrate two distinct neural mechanisms that foster the intentional forgetting of such unwanted memories. Both mechanisms impair long-term retention by limiting momentary awareness of the memories, yet they operate in opposite ways. One mechanism, direct suppression, disengages episodic retrieval through the systemic inhibition of hippocampal processing that originates from right dorsolateral prefrontal cortex (PFC). The opposite mechanism, thought substitution, instead engages retrieval processes to occupy the limited focus of awareness with a substitute memory. It is mediated by interactions between left caudal and midventrolateral PFC that support the selective retrieval of substitutes in the context of prepotent, unwanted memories. These findings suggest that we are not at the mercy of passive forgetting; rather, our memories can be shaped by two opposite mechanisms of mnemonic control.

          Highlights

          ► Voluntarily forgetting is mediated by two opposite mechanisms ► These mechanisms recruit distinct PFC systems to either engage or disengage retrieval ► DLPFC effectively inhibits retrieval processes supported by the hippocampus ► A cPFC-mid-VLPFC circuit biases retrieval to supplant unwanted memories

          Abstract

          Suppressing awareness of an unwanted memory can cause forgetting. Benoit and Anderson show how this motivated forgetting can be achieved by opposite prefrontal mechanisms that either suppress hippocampal retrieval processes or engage retrieval to occupy awareness with a substitute memory.

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          Most cited references41

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          Dynamic causal modelling.

          In this paper we present an approach to the identification of nonlinear input-state-output systems. By using a bilinear approximation to the dynamics of interactions among states, the parameters of the implicit causal model reduce to three sets. These comprise (1) parameters that mediate the influence of extrinsic inputs on the states, (2) parameters that mediate intrinsic coupling among the states, and (3) [bilinear] parameters that allow the inputs to modulate that coupling. Identification proceeds in a Bayesian framework given known, deterministic inputs and the observed responses of the system. We developed this approach for the analysis of effective connectivity using experimentally designed inputs and fMRI responses. In this context, the coupling parameters correspond to effective connectivity and the bilinear parameters reflect the changes in connectivity induced by inputs. The ensuing framework allows one to characterise fMRI experiments, conceptually, as an experimental manipulation of integration among brain regions (by contextual or trial-free inputs, like time or attentional set) that is revealed using evoked responses (to perturbations or trial-bound inputs, like stimuli). As with previous analyses of effective connectivity, the focus is on experimentally induced changes in coupling (cf., psychophysiologic interactions). However, unlike previous approaches in neuroimaging, the causal model ascribes responses to designed deterministic inputs, as opposed to treating inputs as unknown and stochastic.
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            Left ventrolateral prefrontal cortex and the cognitive control of memory.

            Cognitive control mechanisms permit memory to be accessed strategically, and so aid in bringing knowledge to mind that is relevant to current goals and actions. In this review, we consider the contribution of left ventrolateral prefrontal cortex (VLPFC) to the cognitive control of memory. Reviewed evidence supports a two-process model of mnemonic control, supported by a double dissociation among rostral regions of left VLPFC. Specifically, anterior VLPFC (approximately BA 47; inferior frontal gyrus pars orbitalis) supports controlled access to stored conceptual representations, whereas mid-VLPFC (approximately BA 45; inferior frontal gyrus pars triangularis) supports a domain-general selection process that operates post-retrieval to resolve competition among active representations. We discuss the contribution of these control mechanisms across a range of mnemonic domains, including semantic retrieval, recollection of contextual details about past events, resolution of proactive interference in working memory, and task switching. Finally, we consider open directions for future research into left VLPFC function and the cognitive control of memory.
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              Hippocampal replay in the awake state: a potential substrate for memory consolidation and retrieval.

              The hippocampus is required for the encoding, consolidation and retrieval of event memories. Although the neural mechanisms that underlie these processes are only partially understood, a series of recent papers point to awake memory replay as a potential contributor to both consolidation and retrieval. Replay is the sequential reactivation of hippocampal place cells that represent previously experienced behavioral trajectories and occurs frequently in the awake state, particularly during periods of relative immobility. Awake replay may reflect trajectories through either the current environment or previously visited environments that are spatially remote. The repetition of learned sequences on a compressed time scale is well suited to promote memory consolidation in distributed circuits beyond the hippocampus, suggesting that consolidation occurs in both the awake and sleeping animal. Moreover, sensory information can influence the content of awake replay, suggesting a role for awake replay in memory retrieval.
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                Author and article information

                Journal
                Neuron
                Neuron
                Neuron
                Cell Press
                0896-6273
                1097-4199
                18 October 2012
                18 October 2012
                : 76-248
                : 2
                : 450-460
                Affiliations
                [1 ]MRC Cognition and Brain Sciences Unit, 15 Chaucer Road, Cambridge CB2 7EF, UK
                Author notes
                []Corresponding author roland.benoit@ 123456mrc-cbu.cam.ac.uk
                Article
                NEURON11247
                10.1016/j.neuron.2012.07.025
                3480638
                23083745
                fdc6a7ce-a50b-48a9-b0b8-5d2aec159aa8
                © 2012 ELL & Excerpta Medica.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 31 July 2012
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                Neurosciences
                Neurosciences

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