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Generalization and recovery of post-retrieval amnesia.

ABSTRACT: Selective amnesia for previously established memories can be induced by administering drugs that impair protein synthesis shortly after memory reactivation. Competing theoretical accounts attribute this selective post-retrieval amnesia to drug-induced engram degradation (reconsolidation blockade) or to incorporation of sensory features of the reactivation experience into the memory representation, hampering later retrieval in a drug-free state (memory integration). Here we present evidence that critically challenges both accounts. In contextual fear conditioning in rats, we find that amnesia induced by administration of midazolam (MDZ) after reexposure to the training context A generalizes readily to a similar context B. Amnesia is also observed when animals are exposed to the similar context B prior to MDZ administration and later tested for fear to context B but recovers when instead testing for fear to the original training context A or an equally similar but novel context C. Next to their theoretical implications for the nature of forgetting, our findings raise important questions about the viability of reconsolidation-based interventions for the treatment of emotional disorders. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

SUBMITTER: Alfei JM

PROVIDER: S-EPMC7116269 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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Generalization and recovery of post-retrieval amnesia.

Alfei Joaquín M JM Ferrer Monti Roque I RI Molina Victor A VA De Bundel Dimitri D Luyten Laura L Beckers Tom T

Journal of experimental psychology. General 20200416 11

Selective amnesia for previously established memories can be induced by administering drugs that impair protein synthesis shortly after memory reactivation. Competing theoretical accounts attribute this selective post-retrieval amnesia to drug-induced engram degradation (reconsolidation blockade) or to incorporation of sensory features of the reactivation experience into the memory representation, hampering later retrieval in a drug-free state (memory integration). Here we present evidence that ...[more]

PMID: 32297779

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Project description:BackgroundLong-term memory formation is generally assumed to involve the permanent storage of recently acquired memories, making them relatively insensitive to disruption, a process referred to as memory consolidation. However, when retrieved under specific circumstances, consolidated fear memories are thought to return to a labile state, thereby opening a window for modification (e.g., attenuation) of the memory. Several interventions during a critical time frame after this destabilization seem to be able to alter the retrieved memory, for example by pharmacologically interfering with the restabilization process, either by direct protein synthesis inhibition or indirectly, using drugs that can be safely administered in patients (e.g., propranolol). Here, we find that, contrary to expectations, systemic pharmacological manipulations in auditory fear-conditioned rats do not lead to drug-induced post-retrieval amnesia.ResultsIn a series of well-powered auditory fear conditioning experiments (four with propranolol, 10 mg/kg, two with rapamycin, 20-40 mg/kg, one with anisomycin, 150 mg/kg and cycloheximide, 1.5 mg/kg), we found no evidence for reduced cued fear memory expression during a drug-free test in adult male Sprague-Dawley rats that had previously received a systemic drug injection upon retrieval of the tone fear memory. All experiments used standard fear conditioning and reactivation procedures with freezing as the behavioral read-out (conceptual or exact replications of published reports) and common pharmacological agents. Additional tests confirmed that the applied drug doses and administration routes were effective in inducing their conventional effects on expression of fear (propranolol, acutely), body weight (rapamycin, anisomycin, cycloheximide), and consolidation of extinction memories (cycloheximide).ConclusionsIn contrast with previously published studies, we did not find evidence for drug-induced post-retrieval amnesia, underlining that this effect, as well as its clinical applicability, may be considerably more constrained and less readily reproduced than what the current literature would suggest.

Project description:Hypnotic amnesia is a functional dissociation from awareness during which information from specific neural processes is unavailable to consciousness. We test the proposal that changes in topographic patterns of cortical oscillations in upper-alpha (10-12?Hz) band selectively inhibit the recall of memories during hypnotic amnesia by blocking availability of locally processed information at specific points in retrieval. Participants were prescreened for high or low hypnotic susceptibility. Following hypnotic induction, participants were presented with a series of 60 face stimuli and were required to identify affective expressions. Participants received a suggestion for amnesia for these faces. They were then presented with a set of 30 old and 30 new faces and identified each as old or new. Amnesia suggestion was lifted and recall tested using the remaining 30 old faces and another 30 new faces. Exact Low Resolution Brain Electromagnetic Tomography source analyses are reported for 64 channel event-related electroencephalogram recorded from highs showing reversible amnesia to old faces. For high-susceptible participants, the amnesia suggestion significantly increased old faces wrongly identified while for low-susceptible participants amnesia suggestion increased the new faces wrongly identified. There were no differences between high- and low-susceptible participants following reversal of the suggestion. For previously seen faces which were wrongly identified, compared to new faces correctly identified, (late) evoked upper-alpha is significantly higher in right BA7 in a region implicated in top-down executive control to assist recall of visual information. Lagged nonlinear connectivity between cortical sources in upper-alpha in the same condition showed significantly increased connectivity between right BA34 (parahippocampal gyrus) and right BAs 7, 20 and 22. Integration between these regions is essential for recall of recent faces. During amnesia, spatial and temporal coordination of upper-alpha appears to suppress integrated functioning of these regions (hence recall). These patterns were absent after reversal of amnesia suggestion.

Project description:SEE BIGLER DOI101093/AWW277 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Post-traumatic amnesia is very common immediately after traumatic brain injury. It is characterized by a confused, agitated state and a pronounced inability to encode new memories and sustain attention. Clinically, post-traumatic amnesia is an important predictor of functional outcome. However, despite its prevalence and functional importance, the pathophysiology of post-traumatic amnesia is not understood. Memory processing relies on limbic structures such as the hippocampus, parahippocampus and parts of the cingulate cortex. These structures are connected within an intrinsic connectivity network, the default mode network. Interactions within the default mode network can be assessed using resting state functional magnetic resonance imaging, which can be acquired in confused patients unable to perform tasks in the scanner. Here we used this approach to test the hypothesis that the mnemonic symptoms of post-traumatic amnesia are caused by functional disconnection within the default mode network. We assessed whether the hippocampus and parahippocampus showed evidence of transient disconnection from cortical brain regions involved in memory processing. Nineteen patients with traumatic brain injury were classified into post-traumatic amnesia and traumatic brain injury control groups, based on their performance on a paired associates learning task. Cognitive function was also assessed with a detailed neuropsychological test battery. Functional interactions between brain regions were investigated using resting-state functional magnetic resonance imaging. Together with impairments in associative memory, patients in post-traumatic amnesia demonstrated impairments in information processing speed and spatial working memory. Patients in post-traumatic amnesia showed abnormal functional connectivity between the parahippocampal gyrus and posterior cingulate cortex. The strength of this functional connection correlated with both associative memory and information processing speed and normalized when these functions improved. We have previously shown abnormally high posterior cingulate cortex connectivity in the chronic phase after traumatic brain injury, and this abnormality was also observed in patients with post-traumatic amnesia. Patients with post-traumatic amnesia showed evidence of widespread traumatic axonal injury measured using diffusion magnetic resonance imaging. This change was more marked within the cingulum bundle, the tract connecting the parahippocampal gyrus to the posterior cingulate cortex. These findings provide novel insights into the pathophysiology of post-traumatic amnesia and evidence that memory impairment acutely after traumatic brain injury results from altered parahippocampal functional connectivity, perhaps secondary to the effects of axonal injury on white matter tracts connecting limbic structures involved in memory processing.

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Generalization and recovery of post-retrieval amnesia.

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Generalization and recovery of post-retrieval amnesia.

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