Psychedelics and reconsolidation of traumatic and appetitive maladaptive memories: focus on cannabinoids and ketamine
This study (2017) reviews the clinical and preclinical data concerning cannabinoids and ketamine as they relate to possible reconsolidation processes of maladaptive memories.
Authors
- Fattore, L.
- Piva, A.
- Zanda, M. T.
Published
Abstract
Rationale
Clinical data with 3,4-methylenedioxymethamphetamine (MDMA) in post-traumatic stress disorder (PTSD) patients recently stimulated interest on the potential therapeutic use of psychedelics in disorders characterized by maladaptive memories, including substance use disorders (SUD). The rationale for the use of MDMA in PTSD and SUD is being extended to a broader beneficial “psychedelic effect,” which is supporting further clinical investigations, in spite of the lack of mechanistic hypothesis. Considering that the retrieval of emotional memories reactivates specific brain mechanisms vulnerable to inhibition, interference, or strengthening (i.e., the reconsolidation process), it was proposed that the ability to retrieve and change these maladaptive memories might be a novel intervention for PTSD and SUD. The mechanisms underlying MDMA effects indicate memory reconsolidation modulation as a hypothetical process underlying its efficacy.
Objective
Mechanistic and clinical studies with other two classes of psychedelic substances, namely cannabinoids and ketamine, are providing data in support of a potential use in PTSD and SUD based on the modulation of traumatic and appetitive memory reconsolidation, respectively. Here, we review preclinical and clinical data on cannabinoids and ketamine effects on biobehavioral processes related to the reconsolidation of maladaptive memories.
Results
We report the findings supporting (or not) the working hypothesis linking the potential therapeutic effect of these substances to the underlying reconsolidation process. We also proposed possible approaches for testing the use of these two classes of drugs within the current paradigm of reconsolidation memory inhibition.
Conclusions
Metaplasticity may be the process in common between cannabinoids and ketamine/ketamine-like substance effects on the mediation and potential manipulation of maladaptive memories.
Research Summary of 'Psychedelics and reconsolidation of traumatic and appetitive maladaptive memories: focus on cannabinoids and ketamine'
Introduction
Fattore and colleagues open from recent clinical interest in psychedelics sparked by positive results with MDMA in post-traumatic stress disorder (PTSD). They note that MDMA–assisted psychotherapy reduced PTSD symptoms and altered amygdala function, which has stimulated broader interest in using psychedelics to treat disorders characterised by maladaptive emotional memories, including substance use disorders (SUD). The introduction summarises the theoretical shift underpinning these proposals: memories are not immutable but can become labile after retrieval and undergo reconsolidation, a time-limited process during which they may be inhibited, interfered with, or updated. This review sets out to examine whether two classes of psychedelic‑acting substances—cannabinoids (including modulation of the endocannabinoid system) and ketamine—have preclinical and clinical effects that plausibly act via modulation of traumatic or appetitive memory reconsolidation. The authors aim to assemble mechanistic and clinical evidence that supports or contradicts the hypothesis that these agents can therapeutically alter maladaptive memories, and to outline possible translational approaches for testing them in reconsolidation-targeted interventions.
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Study Details
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- APA Citation
Fattore, L., Piva, A., Zanda, M. T., Fumagalli, G., & Chiamulera, C. (2018). Psychedelics and reconsolidation of traumatic and appetitive maladaptive memories: focus on cannabinoids and ketamine. Psychopharmacology, 235(2), 433-445. https://doi.org/10.1007/s00213-017-4793-4
References (8)
Papers cited by this study that are also in Blossom
Amoroso, T., Workman, M. · Journal of Psychopharmacology (2016)
Girgenti, M. J., Ghosal, S., Lopresto, D. et al. · Neurobiology of Disease (2017)
Mcghee, L. L., Maani, C. V., Garza, T. H. et al. · Journal of Trauma Injury Infection and Critical Care (2008)
Mithoefer, M. C., Wagner, M. T., Mithoefer, A. T. et al. · Journal of Psychopharmacology (2012)
Murrough, J. W., Iosifescu, D. V., Chang, L. C. et al. · American Journal of Psychiatry (2013)
Parrott, A. C. · Journal of Psychoactive Drugs (2014)
Yazar-Klosinski, B., Mithoefer, M. C. · Clinical Pharmacology and Therapeutics (2016)
Young, M. B., Andero, R., Ressler, K. J. et al. · Translational Psychiatry (2015)
Cited By (4)
Papers in Blossom that reference this study
Carhart-Harris, R. L., Chandaria, S., Erritzoe, D. E. et al. · Neuropharmacology (2023)
Balaet, M. · Frontiers in Neuroscience (2022)
Norbury, A., Rutter, S. B., Collins, A. B. et al. · Neuropsychopharmacology (2021)
Morgan, L. · Annals of General Psychiatry (2020)
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