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Journal articles on the topic 'Memory reconsolidation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Treanor, Michael, Lily A. Brown, Jesse Rissman, and Michelle G. Craske. "Can Memories of Traumatic Experiences or Addiction Be Erased or Modified? A Critical Review of Research on the Disruption of Memory Reconsolidation and Its Applications." Perspectives on Psychological Science 12, no. 2 (2017): 290–305. http://dx.doi.org/10.1177/1745691616664725.

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Recent research suggests that the mere act of retrieving a memory can temporarily make that memory vulnerable to disruption. This process of “reconsolidation” will typically restabilize the neural representation of the memory and foster its long-term storage. However, the process of reconsolidating the memory takes time to complete, and during this limited time window, the original memory may be modified either by the presentation of new information or with pharmacological agents. Such findings have prompted rising interest in using disruption during reconsolidation as a clinical intervention

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2

Alberini, Cristina M., and Joseph E. LeDoux. "Memory reconsolidation." Current Biology 23, no. 17 (2013): R746—R750. http://dx.doi.org/10.1016/j.cub.2013.06.046.

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3

Gonzalez, María Carolina, Janine I. Rossato, Andressa Radiske, Lia R. M. Bevilaqua, and Martín Cammarota. "Dopamine controls whether new declarative information updates reactivated memories through reconsolidation." Proceedings of the National Academy of Sciences 118, no. 29 (2021): e2025275118. http://dx.doi.org/10.1073/pnas.2025275118.

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Consolidation and reconsolidation are independent memory processes. Consolidation stabilizes new memories, whereas reconsolidation restabilizes memories destabilized when reactivated during recall. However, the biological role of the destabilization/reconsolidation cycle is still unknown. It has been hypothesized that reconsolidation links new information with reactivated memories, but some reports suggest that new and old memories are associated through consolidation mechanisms instead. Object-recognition memory (ORM) serves to judge the familiarity of items and is essential for remembering p

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4

Kida, S. "Roles of CREB Signaling Pathway in Regulation of Fear Memory." European Psychiatry 24, S1 (2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70321-9.

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Activity-dependent gene expression through activation of Ca2+-CREB signal transduction pathways has been thought to play a central role in fear memory formation. On the other hand, retrieval of fear memory triggers two time-dependent phases of reactivated memory; reconsolidation and extinction. To understand the mechanisms for determining the fate of the reactivated fear memory, we investigated roles of CREB in reconsolidation and extinction of contextual fear memory and then analyzed the brain-regions regulating reconsolidation and extinction by identifying regions where CREB-mediated gene ex

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Child, F. M., H. T. Epstein, A. M. Kuzirian, and D. L. Alkon. "Memory Reconsolidation inHermissenda." Biological Bulletin 205, no. 2 (2003): 218–19. http://dx.doi.org/10.2307/1543261.

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6

Ecker, Bruce. "UNDERSTANDING MEMORY RECONSOLIDATION." Neuropsychotherapist, no. 10 (January 1, 2015): 4–22. http://dx.doi.org/10.12744/tnpt(10)004-022.

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7

Rabinovich Orlandi, Iván, Camila L. Fullio, Matías Nicolás Schroeder, Martin Giurfa, Fabricio Ballarini, and Diego Moncada. "Behavioral tagging underlies memory reconsolidation." Proceedings of the National Academy of Sciences 117, no. 30 (2020): 18029–36. http://dx.doi.org/10.1073/pnas.2009517117.

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Memory reconsolidation occurs when a retrieving event destabilizes transiently a consolidated memory, triggering thereby a new process of restabilization that ensures memory persistence. Although this phenomenon has received wide attention, the effect of new information cooccurring with the reconsolidation process has been less explored. Here we demonstrate that a memory-retrieving event sets a neural tag, which enables the reconsolidation of memory after binding proteins provided by the original or a different contiguous experience. We characterized the specific temporal window during which t

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Liu, Xing, Li Ma, Hao Hong Li та ін. "β-Arrestin–biased signaling mediates memory reconsolidation". Proceedings of the National Academy of Sciences 112, № 14 (2015): 4483–88. http://dx.doi.org/10.1073/pnas.1421758112.

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A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and memory. Here we report that memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation memory restabilization. β-Arrestin2-deficient mice exhibit impaired memory reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenerg

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Elahi, Hajira, Veronica Hong, and Jonathan E. Ploski. "Electroconvulsive Shock Does Not Impair the Reconsolidation of Cued and Contextual Pavlovian Threat Memory." International Journal of Molecular Sciences 21, no. 19 (2020): 7072. http://dx.doi.org/10.3390/ijms21197072.

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Existing memories, when retrieved under certain circumstances, can undergo modification through the protein synthesis-dependent process of reconsolidation. Disruption of this process can lead to the weakening of a memory trace, an approach which is being examined as a potential treatment for disorders characterized by pathological memories, such as Post-Traumatic Stress Disorder. The success of this approach relies upon the ability to robustly attenuate reconsolidation; however, the available literature brings into question the reliability of the various drugs used to achieve such a blockade.

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10

Galarza Vallejo, Ana, Marijn C. W. Kroes, Enrique Rey, et al. "Propofol-induced deep sedation reduces emotional episodic memory reconsolidation in humans." Science Advances 5, no. 3 (2019): eaav3801. http://dx.doi.org/10.1126/sciadv.aav3801.

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The adjustment of maladaptive thoughts and behaviors associated with emotional memories is central to treating psychiatric disorders. Recent research, predominantly with laboratory animals, indicates that memories can become temporarily sensitive to modification following reactivation, before undergoing reconsolidation. A method to selectively impair reconsolidation of specific emotional or traumatic memories in humans could translate to an effective treatment for conditions such as posttraumatic stress disorder. We tested whether deep sedation could impair emotional memory reconsolidation in

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11

Hardwicke, Tom E., Mahdi Taqi, and David R. Shanks. "Postretrieval new learning does not reliably induce human memory updating via reconsolidation." Proceedings of the National Academy of Sciences 113, no. 19 (2016): 5206–11. http://dx.doi.org/10.1073/pnas.1601440113.

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Reconsolidation theory proposes that retrieval can destabilize an existing memory trace, opening a time-dependent window during which that trace is amenable to modification. Support for the theory is largely drawn from nonhuman animal studies that use invasive pharmacological or electroconvulsive interventions to disrupt a putative postretrieval restabilization (“reconsolidation”) process. In human reconsolidation studies, however, it is often claimed that postretrieval new learning can be used as a means of “updating” or “rewriting” existing memory traces. This proposal warrants close scrutin

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12

Bellfy, Lauren, and Janine L. Kwapis. "Molecular Mechanisms of Reconsolidation-Dependent Memory Updating." International Journal of Molecular Sciences 21, no. 18 (2020): 6580. http://dx.doi.org/10.3390/ijms21186580.

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Memory is not a stable record of experience, but instead is an ongoing process that allows existing memories to be modified with new information through a reconsolidation-dependent updating process. For a previously stable memory to be updated, the memory must first become labile through a process called destabilization. Destabilization is a protein degradation-dependent process that occurs when new information is presented. Following destabilization, a memory becomes stable again through a protein synthesis-dependent process called restabilization. Much work remains to fully characterize the

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13

Kiley, Christopher, and Colleen M. Parks. "Generalising reconsolidation: Spatial context and prediction error." Quarterly Journal of Experimental Psychology 73, no. 11 (2020): 1745–56. http://dx.doi.org/10.1177/1747021820922555.

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Activating a previously consolidated memory trace brings it back into a labile state where it must then undergo a re-stabilisation process known as reconsolidation. During this process memories are susceptible to interference and may be updated with new information. In the studies showing this effect in human episodic memory, the reconsolidation process has been triggered primarily using spatial context or prediction error manipulations to reactivate an established memory. However, these studies have produced conflicting results, showing both that spatial context is necessary and sufficient to

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Navabpour, Shaghayegh, Jessie Rogers, Taylor McFadden, and Timothy J. Jarome. "DNA Double-Strand Breaks Are a Critical Regulator of Fear Memory Reconsolidation." International Journal of Molecular Sciences 21, no. 23 (2020): 8995. http://dx.doi.org/10.3390/ijms21238995.

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Numerous studies have shown that following retrieval, a previously consolidated memory requires increased transcriptional regulation in order to be reconsolidated. Previously, it was reported that histone H3 lysine-4 trimethylation (H3K4me3), a marker of active transcription, is increased in the hippocampus after the retrieval of contextual fear memory. However, it is currently unknown how this epigenetic mark is regulated during the reconsolidation process. Furthermore, though recent evidence suggests that neuronal activity triggers DNA double-strand breaks (DSBs) in some early-response genes

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15

Lee, Jonathan L. C. "Reconsolidation: maintaining memory relevance." Trends in Neurosciences 32, no. 8 (2009): 413–20. http://dx.doi.org/10.1016/j.tins.2009.05.002.

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16

Piskała, Kamil. "Socialist postcolonialism: memory reconsolidation." Journal of Contemporary Central and Eastern Europe 27, no. 2-3 (2019): 286–88. http://dx.doi.org/10.1080/25739638.2019.1694249.

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17

Nader, Karim, and Einar Örn Einarsson. "Memory reconsolidation: an update." Annals of the New York Academy of Sciences 1191, no. 1 (2010): 27–41. http://dx.doi.org/10.1111/j.1749-6632.2010.05443.x.

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18

Ecker, Bruce. "memory reconsolidation in NLP." Neuropsychotherapist, no. 10 (January 1, 2015): 50–56. http://dx.doi.org/10.12744/tnpt(10)050-056.

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19

Campbell, Tiffany L., Daniel E. Kochli, Mitch A. McDaniel, et al. "Using Extinction-Renewal to Circumvent the Memory Strength Boundary Condition in Fear Memory Reconsolidation." Brain Sciences 11, no. 8 (2021): 1023. http://dx.doi.org/10.3390/brainsci11081023.

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Reconsolidation is a process by which memories are destabilized, updated, and then restabilized. Strong memories are resistant to undergoing reconsolidation. Here, we addressed whether an overtrained fear memory could be made susceptible to reconsolidation by first extinguishing, and then renewing, the memory. Rats were trained with ten tone-footshock pairings, followed by eight days of tone extinction in the training context. The next day, rats were placed into a second context and memory for the tone was renewed/reactivated with a single tone presentation. Immediately following reactivation,

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20

Manenti, Rosa, Marco Sandrini, Elena Gobbi, Giuliano Binetti, and Maria Cotelli. "Effects of Transcranial Direct Current Stimulation on Episodic Memory in Amnestic Mild Cognitive Impairment: A Pilot Study." Journals of Gerontology: Series B 75, no. 7 (2018): 1403–13. http://dx.doi.org/10.1093/geronb/gby134.

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Abstract Objectives Episodic memory is impaired in amnestic mild cognitive impairment (aMCI), which is posited as a potential prodromal form of Alzheimer’s disease. Reactivated existing memories become sensitive to modification during reconsolidation. There is evidence that the lateral prefrontal cortex (PFC) plays causal role in episodic memory reconsolidation. Transcranial direct current stimulation (tDCS) applied to the PFC after a contextual reminder enhanced episodic memory performance up to 1 month, conceivably through reconsolidation, in older adults with subjective memory complaints, a

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21

Balaban, P. M., and A. A. Borodinova. "Time and memory." Zhurnal Vysshei Nervnoi Deyatelnosti Imeni I.P. Pavlova 74, no. 6 (2024): 657–66. https://doi.org/10.31857/s0044467724060023.

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In this review, based on our own and literature data, the temporal course of long-term memory formation, the duration of consolidation and reconsolidation processes, the temporal parameters of the interaction of glial and neuronal elements of the neural network, and possible mechanisms of neuro-glial interactions are analyzed. Based on the analysis, an assumption was made that allows us to explain the duration of the period of consolidation and reconsolidation of long-term memory (4–6 hours) by the need for the contribution of glia to the local epigenetic regulation of plasticity gene expressi

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22

Liu, Peng, Jialong Liang, Fengze Jiang, et al. "Gnas Promoter Hypermethylation in the Basolateral Amygdala Regulates Reconsolidation of Morphine Reward Memory in Rats." Genes 13, no. 3 (2022): 553. http://dx.doi.org/10.3390/genes13030553.

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Impairing reconsolidation may disrupt drug memories to prevent relapse, meanwhile long-term transcription regulations in the brain regions contribute to the occurrence of emotional memories. The basolateral amygdala (BLA) is involved in the drug-cue association, while the nucleus accumbens (NAc) responds to the drug reward. Here, we assessed whether DNA methyltransferases (Dnmts) in these two brain regions function identically in the reconsolidation of morphine reward memory. We show that Dnmts inhibition in the BLA but not in the NAc after memory retrieval impaired reconsolidation of a morphi

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23

Shu, Hui, Mengwei Wang, Min Song, et al. "Acute Nicotine Treatment Alleviates LPS-Induced Impairment of Fear Memory Reconsolidation Through AMPK Activation and CRTC1 Upregulation in Hippocampus." International Journal of Neuropsychopharmacology 23, no. 10 (2020): 687–99. http://dx.doi.org/10.1093/ijnp/pyaa043.

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Abstract Background Fear memory is a fundamental capability for animals and humans to survive. Its impairment results in the disability to avoid danger. When memory is reactivated, a reconsolidation process, which can be disrupted by various stimuli, including inflammation, is required to become permanent. Nicotine has been shown to improve cognitive deficits induced by inflammation and other stimuli. Therefore, in the present study, we investigated the effect of nicotine on lipopolysaccharide (LPS)-induced impairment of fear memory reconsolidation and the underlying mechanism. Methods Step-th

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Kindt, Merel. "The surprising subtleties of changing fear memory: a challenge for translational science." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1742 (2018): 20170033. http://dx.doi.org/10.1098/rstb.2017.0033.

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Current pharmacological and psychological treatments for disorders of emotional memory only dampen the affective response while leaving the original fear memory intact. Under adverse circumstances, these original memories regain prominence, causing relapses in many patients. The (re)discovery in neuroscience that after reactivation consolidated fear memories may return to a transient labile state, requiring a process of restabilization in order to persist, offers a window of opportunity for modifying fear memories with amnestic agents. This process, known as memory reconsolidation, opens avenu

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Nitta, Yusuke, Toru Takahashi, Tomosumi Haitani, Eriko Sugimori, and Hiroaki Kumano. "Avoidance Behavior Prevents Modification of Fear Memory During Reconsolidation." Psychological Reports 123, no. 2 (2018): 224–38. http://dx.doi.org/10.1177/0033294118811116.

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Several studies have revealed that fear recovery is prevented when extinction training is conducted after retrieval of a fear memory. Postretrieval extinction training is related to modification of memory during reconsolidation. Providing new information during reconsolidation can modify the original memory. We propose that avoidance behavior is a relevant factor that prevents subjects from obtaining new safety information during reconsolidation. Postretrieval extinction training without avoidance behavior reduced the fear response to conditioned stimulus and prevented spontaneous recovery in

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26

Yu, Moon Hee. "Research Trends in Korea Counseling Field on the Application of Neuroscientific Memory Reconsolidation: A Scoping Review." Asia Counseling and Coaching Society 6, no. 1 (2024): 1–15. https://doi.org/10.47018/accr.2024.6.1.1.

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This research aimed to examine the direction of research on the mechanisms of memory reconsolidation as a view of neuroscientific discovery in the counseling field through a scoping review in Korea. For this purpose, it was searched through electronic databases. It finally extracted six out of sixty-one papers from literature published in Korea from 2012 to 2023 according to the selection criteria. As a result of the research, although various psychological states were explained in the counseling field as a memory reconsolidation mechanism, access to and utilization of multidisciplinary neuros

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Grigoryan, G. A. "Neuroinflammation and Reconsolidation of Memory." Neurochemical Journal 16, no. 2 (2022): 109–20. http://dx.doi.org/10.1134/s1819712422020076.

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28

Loprinzi, Paul D., Ashley Lovorn, Emma Hamilton, and Noelle Mincarelli. "Acute Exercise on Memory Reconsolidation." Journal of Clinical Medicine 8, no. 8 (2019): 1200. http://dx.doi.org/10.3390/jcm8081200.

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Background and Objective: Once a memory is reactivated, it enters a labile state and, thus, is vulnerable to memory decay and/or distortion. Recent research demonstrates that acute, high-intensity exercise is associated with enhanced episodic memory function. Very limited research, however, has evaluated whether acute exercise can attenuate memory distortion from memory reactivation, which was the purpose of this study. Methods: A between-subject randomized controlled intervention was employed. Participants (N = 80) were randomly assigned to one of four groups, including (1) reminder with exer

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Duvarci, S. "Characterization of Fear Memory Reconsolidation." Journal of Neuroscience 24, no. 42 (2004): 9269–75. http://dx.doi.org/10.1523/jneurosci.2971-04.2004.

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30

Tronson, Natalie C., and Jane R. Taylor. "Molecular mechanisms of memory reconsolidation." Nature Reviews Neuroscience 8, no. 4 (2007): 262–75. http://dx.doi.org/10.1038/nrn2090.

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31

De Jaeger, X., J. Courtey, M. Brus, et al. "Characterization of spatial memory reconsolidation." Learning & Memory 21, no. 6 (2014): 316–24. http://dx.doi.org/10.1101/lm.033415.113.

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32

Bustos, S. G., H. Maldonado, and V. A. Molina. "Midazolam disrupts fear memory reconsolidation." Neuroscience 139, no. 3 (2006): 831–42. http://dx.doi.org/10.1016/j.neuroscience.2005.12.064.

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JOHNSON, KATE. "PTSD Research Targets Memory Reconsolidation." Clinical Psychiatry News 39, no. 1 (2011): 12. http://dx.doi.org/10.1016/s0270-6644(11)70060-1.

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34

Ecker, Bruce. "Memory reconsolidation understood and misunderstood." International Journal of Neuropsychotherapy 3, no. 1 (2015): 2–46. http://dx.doi.org/10.12744/ijnpt.2015.0002-0046.

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35

Lasser, Kymberly, and Ricky Greenwald. "Progressive counting facilitates memory reconsolidation." Neuropsychotherapist, no. 10 (January 1, 2015): 30–37. http://dx.doi.org/10.12744/tnpt(10)030-037.

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Zyuzina, A. B., and P. M. Balaban. "Extinction and Reconsolidation of Memory." Neuroscience and Behavioral Physiology 47, no. 1 (2016): 74–82. http://dx.doi.org/10.1007/s11055-016-0367-x.

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37

Simon, Katharine C., Rebecca L. Gómez, and Lynn Nadel. "Sleep’s role in memory reconsolidation." Current Opinion in Behavioral Sciences 33 (June 2020): 132–37. http://dx.doi.org/10.1016/j.cobeha.2020.04.001.

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38

Zuzina, А. B., and P. М. Balaban. "THE CONTRIBUTION OF EPIGENETIC MECHANISMS TO THE FORMATION, MAINTENANCE AND RECONSOLIDATION OF THE LONG-TERM FOOD AVERSIVE MEMORY IN TERRESTRIAL SNAIL." Журнал высшей нервной деятельности им. И.П. Павлова 73, no. 5 (2023): 688–703. http://dx.doi.org/10.31857/s0044467723050118.

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This work was devoted to the analysis of the role of epigenetic mechanisms (histone acetylation, DNA methylation, histone serotonylation) in the formation, storage, and reconsolidation of long-term food aversive memory in the snail. In the first part of the work, we investigated the effect of systemic administration of sodium butyrate, an inhibitor of histone deacetylase, in a model of conditioned food aversion reflex of the snail. We have shown that the administration of sodium butyrate to animals with poor memory resulted in memory enhancement. Further, in experiments using the DNA methyltra

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Zhao, Hongyi, Dandan Li, and Xiuzhen Li. "Relationship between Dreaming and Memory Reconsolidation." Brain Science Advances 4, no. 2 (2018): 118–30. http://dx.doi.org/10.26599/bsa.2018.9050005.

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Dreaming is a ubiquitous phenomenon in human beings and has been discussed, researched, and hypothesized since a long time. The substrate, physiological mechanism, and function of dreaming have been explained by many scientists from the neurological, psychiatric, psychological, and philosophical perspective. With the development of scientific technology, many theories of dreaming have been established. In the present review, we first summarize the different theories of dreaming; furthermore, we introduce memory consolidation and reconsolidation. Lastly, we propose that memory might be associat

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Barak, Segev, and Koral Goltseker. "Targeting the Reconsolidation of Licit Drug Memories to Prevent Relapse: Focus on Alcohol and Nicotine." International Journal of Molecular Sciences 22, no. 8 (2021): 4090. http://dx.doi.org/10.3390/ijms22084090.

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Alcohol and nicotine are widely abused legal substances worldwide. Relapse to alcohol or tobacco seeking and consumption after abstinence is a major clinical challenge, and is often evoked by cue-induced craving. Therefore, disruption of the memory for the cue–drug association is expected to suppress relapse. Memories have been postulated to become labile shortly after their retrieval, during a “memory reconsolidation” process. Interference with the reconsolidation of drug-associated memories has been suggested as a possible strategy to reduce or even prevent cue-induced craving and relapse. H

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Ertl, Sebastian, Dagmar Steinmair, Pia Patricia Wadowski, and Henriette Löffler-Stastka. "WHAT WE NEED FOR ENCODING OF MEMORY AND EMOTIONAL RECONSOLIDATION." PSYCHIATRIA DANUBINA 34, no. 2 (2022): 209–18. http://dx.doi.org/10.24869/psyd.2022.209.

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Deryabina, Irina B., Viatcheslav V. Andrianov, Lyudmila N. Muranova, Tatiana K. Bogodvid, and Khalil L. Gainutdinov. "Effects of Thryptophan Hydroxylase Blockade by P-Chlorophenylalanine on Contextual Memory Reconsolidation after Training of Different Intensity." International Journal of Molecular Sciences 21, no. 6 (2020): 2087. http://dx.doi.org/10.3390/ijms21062087.

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The processes of memory formation and its storage are extremely dynamic. Therefore, the determination of the nature and temporal evolution of the changes that underlie the molecular mechanisms of retrieval and cause reconsolidation of memory is the key to understanding memory formation. Retrieval induces the plasticity, which may result in reconsolidation of the original memory and needs critical molecular events to stabilize the memory or its extinction. 4-Chloro-DL-phenylalanine (P-chlorophenylalanine-PCPA) depresses the most limiting enzyme of serotonin synthesis the tryptophan hydroxylase.

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Gonzalez, Maria Carolina, Andressa Radiske, Sergio Conde-Ocazionez, Janine I. Rossato, Lia R. M. Bevilaqua, and Martín Cammarota. "Reactivation-dependent amnesia for object recognition memory is contingent on hippocampal theta–gamma coupling during recall." Learning & Memory 29, no. 1 (2021): 1–6. http://dx.doi.org/10.1101/lm.053482.121.

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Hippocampal dopamine D1/D5 receptor-dependent destabilization is necessary for object recognition memory (ORM) updating through reconsolidation. Dopamine also regulates hippocampal theta and gamma oscillations, which are involved in novelty and memory processing. We found that, in adult male rats, ORM recall in the presence of a novel object, but not in the presence of a familiar one, triggers hippocampal theta–gamma coupling. Hippocampal theta–gamma coupling (hPAC) does not happen when ORM destabilization is prevented by blocking D1/D5 receptors, but artificial hPAC generation during recall i

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Barreiro, Karina A., Luis D. Suárez, Victoria M. Lynch, Víctor A. Molina, and Alejandro Delorenzi. "Memory expression is independent of memory labilization/reconsolidation." Neurobiology of Learning and Memory 106 (November 2013): 283–91. http://dx.doi.org/10.1016/j.nlm.2013.10.006.

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Yeh, Ting-Kuang, Chun-Yen Chang, Mei-Hsin Lin, et al. "Reconsolidation-induced memory disruption in humans declarative memory." Neuroscience Research 65 (January 2009): S191. http://dx.doi.org/10.1016/j.neures.2009.09.1032.

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Fernández, Rodrigo S., María E. Pedreira, and Mariano M. Boccia. "Does reconsolidation occur in natural settings? Memory reconsolidation and anxiety disorders." Clinical Psychology Review 57 (November 2017): 45–58. http://dx.doi.org/10.1016/j.cpr.2017.08.004.

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47

Rahamim, Nofar, Mirit Liran, Coral Aronovici, et al. "Inhibition of ERK1/2 or CRMP2 Disrupts Alcohol Memory Reconsolidation and Prevents Relapse in Rats." International Journal of Molecular Sciences 25, no. 10 (2024): 5478. http://dx.doi.org/10.3390/ijms25105478.

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Relapse to alcohol abuse, often caused by cue-induced alcohol craving, is a major challenge in alcohol addiction treatment. Therefore, disrupting the cue-alcohol memories can suppress relapse. Upon retrieval, memories transiently destabilize before they reconsolidate in a process that requires protein synthesis. Evidence suggests that the mammalian target of rapamycin complex 1 (mTORC1), governing the translation of a subset of dendritic proteins, is crucial for memory reconsolidation. Here, we explored the involvement of two regulatory pathways of mTORC1, phosphoinositide 3-kinase (PI3K)-AKT

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Radiske, Andressa, Maria Carolina Gonzalez, Diana A. Nôga, Janine I. Rossato, Lia R. M. Bevilaqua, and Martín Cammarota. "mTOR inhibition impairs extinction memory reconsolidation." Learning & Memory 28, no. 1 (2020): 1–6. http://dx.doi.org/10.1101/lm.052068.120.

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Forcato, C., V. L. Burgos, P. F. Argibay, V. A. Molina, M. E. Pedreira, and H. Maldonado. "Reconsolidation of declarative memory in humans." Learning & Memory 14, no. 4 (2007): 295–303. http://dx.doi.org/10.1101/lm.486107.

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Gisquet-Verrier, P., and D. C. Riccio. "Memory reactivation effects independent of reconsolidation." Learning & Memory 19, no. 9 (2012): 401–9. http://dx.doi.org/10.1101/lm.026054.112.

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