Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear
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The last 10 years have witnessed a surge of interest for the mechanisms underlying the acquisition and extinction of classically conditioned fear responses. In part, this results from the realization that abnormalities in fear learning mechanisms likely participate in the development and/or maintenance of human anxiety disorders. The simplicity and robustness of this learning paradigm, coupled with the fact that the underlying circuitry is evolutionarily well conserved, make it an ideal model to study the basic biology of memory and identify genetic factors and neuronal systems that regulate the normal and pathological expressions of learned fear. Critical advances have been made in determining how modified neuronal functions upon fear acquisition become stabilized during fear memory consolidation and how these processes are controlled in the course of fear memory extinction. With these advances came the realization that activity in remote neuronal networks must be coordinated for these events to take place. In this paper, we review these mechanisms of coordinated network activity and the molecular cascades leading to enduring fear memory, and allowing for their extinction. We will focus on Pavlovian fear conditioning as a model and the amygdala as a key component for the acquisition and extinction of fear responses.
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The amygdala has a role in threat-responding for social anxiety disorder.
“given its role in threat-responding for social anxiety disorder (Pape and Pare, 2010)”
From Self-referential processing during observation of a speech performance task in social anxiety disorder from pre- to post-treatment: Evidence of disrupted neural activation (2019) · cites this paper as Pape and Pare, 2010
The Introduction identifies the amygdala as a key region for processing aversive signals and fear learning in humans, and discusses abnormal fear responses in anxiety disorders. It does not specifically establish the amygdala’s role in threat-responding in social anxiety disorder. No page numbers were provided in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPost-encoding processes induce synaptic changes, including long-term potentiation (LTP), necessary for stabilization of a memory trace in the hours after acquisition.
“Post-encoding processes account for this dissociation, as they induce the synaptic changes, including long-term potentiation (LTP), that are necessary for the stabilization of a memory trace in the hours after its acquisition [83,84].”
From Multiple memory systems, multiple time points: How science can inform treatment to control the expression of unwanted emotional memories (2018) · cites this paper as [84]
Other learning processes have been connected to brain mechanisms in animal Pavlovian conditioning experiments.
“a variety of other learning processes (e.g., extinction retention, consolidation, reconsolidation, contextual conditioning, reversal, discrimination/generalization) have been linked to brain mechanisms with lab-based Pavlovian conditioning experiments in animals (for a review see9,10).”
There is evidence for increased activation of the amygdala in humans and rodents during conditioned fear.
“There is evidence for increased activation of the amygdala in humans and rodents during conditioned fear (156).”
From Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders (2018) · cites this paper as [156]
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- Authors
- Pape, H.-C., & Pare, D.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- Institute of Physiology, Westfaelische Wilhelms-University, Muenster, Germany; and Rutgers State University, Newark, New Jersey
- Corresponding author
- Pape, Hans-Christian
- ORCID
- Pape, Hans-Christian
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2010-04
- Volume
- 90
- Issue
- 2
- Pages
- 419-463
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- PMC
- PMC2856122
- OpenAlex
- W2076445235
- Cited by
- 994
- References
- 554
- Citations by year
- 2026: 19 · 2025: 28 · 2024: 36 · 2023: 43 · 2022: 40 · 2021: 60 · 2020: 58 · 2019: 61 · 2018: 64 · 2017: 63 · 2016: 79 · 2015: 97 · 2014: 88 · 2013: 85 · 2012: 84
- FWCI
- 5.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Physiological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01MH073610, R01MH083710)
- 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 › Neurobiology and Insect Physiology Research
- Keywords
- amygdala, fear conditioning, fear extinction, fear memory consolidation, anxiety disorders, synaptic plasticity, neuronal network activity
- MeSH terms
- Amygdala, Animals, Anxiety, Extinction, Psychological, Fear, Humans, Nerve Net, Neuronal Plasticity
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