Cited by 174Memory and Neural MechanismsNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

Pharmacological treatments that facilitate extinction of fear: Relevance to psychotherapy

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Davis, Michael, Myers, Karyn M., Chhatwal, Jasmeer, Ressler, Kerry J.·2006·NeuroRX

Abstract

Summary A great deal is now known about the mechanisms of conditioned fear acquisition and expression. More recently, the mechanisms of inhibition of conditioned fear have become the subject of intensive study. The major model system for the study of fear inhibition in the laboratory is extinction, in which a previously fear conditioned organism is exposed repeatedly to the fear-eliciting cue in the absence of any aversive event and the fear conditioned response declines. It is well established that extinction is a form of new learning as opposed to forgetting or "unlearning" of conditioned fear, and it is hypothesized that extinction develops when sensory pathways conveying sensory information to the amygdala come to engage GABAergic interneurons through forms of experience-dependent plasticity such as long-term potentiation. Several laboratories currently are investigating methods of facilitating fear extinction in animals with the hope that such treatments might ultimately prove to be useful in facilitating exposure-based therapy for anxiety disorders in clinical populations. This review discusses the advances that have been made in this field and presents the findings of the first major clinical study to examine the therapeutic utility of a drug that facilitates extinction in animals. It is concluded that extinction is an excellent model system for the study of fear inhibition and an indispensable tool for the screening of putative pharmacotherapies for clinical use.

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Crossref · 10.1016/j.nurx.2005.12.008

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  • Chemically blocking the receptor shortly before extinction training blocks extinction in animal research, showing a dose-response relation.

    “Chemically blocking the receptor shortly before extinction training blocks extinction in animal research, a finding that shows a dose-response relation.”

    From Mediators and Mechanisms of Change in Psychotherapy Research (2007) · cites this paper as Davis et al. 2006

  • Blocking the receptor after extinction training also blocks extinction, suggesting that the consolidation process can be interrupted.

    “Blocking the receptor after extinction training also blocks extinction, which suggests that the consolidation process can be interrupted.”

    From Mediators and Mechanisms of Change in Psychotherapy Research (2007) · cites this paper as Davis et al. 2006

  • Conditioning and extinction of fear depend on a particular receptor in the amygdala, N-methyl-D-aspartate.

    “Conditioning and extinction of fear depend on a particular receptor in the amygdala (N-methyl-D-aspartate) (see Davis et al. 2006).”

    From Mediators and Mechanisms of Change in Psychotherapy Research (2007) · cites this paper as Davis et al. 2006

  • D-cycloserine binds to the receptor and enhances extinction when given before or soon after extinction training.

    “A compound (D-cycloserine) binds to the receptor and makes the receptor work better, i.e., enhances extinction when given before or soon after extinction training.”

    From Mediators and Mechanisms of Change in Psychotherapy Research (2007) · cites this paper as Davis et al. 2006

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1 of the 93 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Davis M, File SE. Intrinsic and extrinsic habituation and sensiti- zation: implications for the design and interpretation of experi- ments. In: Habituation and the behaving organism (Peeke H, Pet- rinovich L, eds), pp 287-323. New York: Academic Press, 1984.
  2. Pavlov I. Conditioned reflexes. Oxford: Oxford University Press, 1927.

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Authors
Davis, M., Myers, K. M., Chhatwal, J., & Ressler, K. J.
Affiliations
Emory University (US)
Corresponding author
Davis, Michael
Venue
NeuroRX
Published
2006-01
Volume
3
Issue
1
Pages
82-96
ISSN
1545-5343 (ISSN-L)
OpenAlex
W1988011200
Cited by
174
References
93
Citations by year
2026: 2 · 2025: 3 · 2024: 4 · 2023: 1 · 2022: 2 · 2021: 27 · 2020: 3 · 2019: 2 · 2018: 5 · 2017: 5 · 2016: 8 · 2015: 7 · 2014: 8 · 2013: 15 · 2012: 15
FWCI
1.31
Type
journal article
Language
en
Open access
Locations
  • NeuroRx (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • Emory University
  • National Institute of Mental Health (MH-047840, MH069884, F30MH070218, MH070218, K01MH069884)
  • National Institute of General Medical Sciences (T32GM008169)
  • National Center for Research Resources (P51RR000165)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
fear extinction, fear conditioning, anxiety disorders, exposure therapy, amygdala, GABAergic interneurons, long-term potentiation, experience-dependent plasticity, fear inhibition
MeSH terms
Extinction, Psychological, Fear, Humans, Phobic Disorders, Psychotherapy, Receptors, Glutamate, Excitatory Amino Acid Agonists, Glutamic Acid

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