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Cited by 137Posttraumatic Stress Disorder ResearchMemory and Neural MechanismsMemory Processes and Influences

Revisiting propranolol and PTSD: Memory erasure or extinction enhancement?

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Giustino, Thomas F., Fitzgerald, Paul J., Maren, Stephen·2016·Neurobiology of Learning and Memory
DOI 10.1016/j.nlm.2016.01.009PMC PMC4818733
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Abstract

Posttraumatic stress disorder (PTSD) has been described as the only neuropsychiatric disorder with a known cause, yet effective behavioral and pharmacotherapies remain elusive for many afflicted individuals. PTSD is characterized by heightened noradrenergic signaling, as well as a resistance to extinction learning. Research aimed at promoting more effective treatment of PTSD has focused on memory erasure (disrupting reconsolidation) and/or enhancing extinction retention through pharmacological manipulations. Propranolol, a β-adrenoceptor antagonist, has received considerable attention for its therapeutic potential in PTSD, although its impact on patients is not always effective. In this review, we briefly examine the consequences of β-noradrenergic manipulations on both reconsolidation and extinction learning in rodents and in humans. We suggest that propranolol is effective as a fear-reducing agent when paired with behavioral therapy soon after trauma when psychological stress is high, possibly preventing or dampening the later development of PTSD. In individuals who have already suffered from PTSD for a significant period of time, propranolol may be less effective at disrupting reconsolidation of strong fear memories. Also, when PTSD has already developed, chronic treatment with propranolol may be more effective than acute intervention, given that individuals with PTSD tend to experience long-term, elevated noradrenergic hyperarousal.

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  • The procedures in Brunet et al.'s study may have been effective because they led to enhanced extinction rather than to memory reconsolidation.

    “In Brunet et al.’s (2018) study, there was extended exposure to the traumatic memories on multiple occasions, raising the possibility that the procedures were effective because they led to enhanced extinction rather than to memory reconsolidation [57].”

    From Memory and Forgetting (2018) · cites this paper as [57]

    Section 2.2 (Humans; page unavailable) says that multiple drug-reactivation sessions in earlier Brunet studies make it difficult to distinguish disrupted reconsolidation from extinction-like processes. That supports the proposed alternative mechanism, but this 2016 paper cannot assess the procedures or effectiveness of Brunet et al.’s 2018 study specifically. (LLM, conf=0.88)

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  • In Brunet et al.'s (2018) study, there was extended exposure to the traumatic memories on multiple occasions.

    “In Brunet et al.’s (2018) study, there was extended exposure to the traumatic memories on multiple occasions, raising the possibility that the procedures were effective because they led to enhanced extinction rather than to memory reconsolidation [57].”

    From Memory and Forgetting (2018) · cites this paper as [57]

    The Introduction (page unavailable) distinguishes brief memory reactivation in reconsolidation studies from the many presentations used in extinction learning, supporting the proposed alternative mechanism. But this 2016 paper does not describe Brunet et al.’s 2018 study, so it cannot verify that study’s extended exposure on multiple occasions. (LLM, conf=0.88)

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Cited by

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Authors
Giustino, T. F., Fitzgerald, P. J., & Maren, S.
Affiliations
Texas A&M University (US)
Corresponding author
Maren, Stephen
ORCID
Venue
Neurobiology of Learning and Memory
Publisher
Elsevier BV
Published
2016-04
Volume
130
Pages
26-33
ISSN
1074-7427 (ISSN-L)
DOI
10.1016/j.nlm.2016.01.009
PMC
PMC4818733
OpenAlex
W2285127741
Cited by
137
References
22
Citations by year
2026: 5 · 2025: 8 · 2024: 8 · 2023: 14 · 2022: 16 · 2021: 21 · 2020: 13 · 2019: 14 · 2018: 18 · 2017: 17 · 2016: 3
FWCI
2.46
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neurobiology of Learning and Memory (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Mental Health (R01MH065961)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
Keywords
propranolol, post-traumatic stress disorder, memory reconsolidation, fear extinction, beta-adrenoceptor antagonism, fear memory, PTSD pharmacotherapy, psychological stress
MeSH terms
Adrenergic beta-Antagonists, Animals, Behavior, Animal, Disease Models, Animal, Extinction, Psychological, Fear, Humans, Memory, Propranolol, Stress Disorders, Post-Traumatic, Rats

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