The structural and functional connectivity of the amygdala: from normal emotion to pathological anxiety
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The dynamic interactions between the amygdala and the medial prefrontal cortex (mPFC) are usefully conceptualized as a circuit that both allows us to react automatically to biologically relevant predictive stimuli as well as regulate these reactions when the situation calls for it. In this review, we will begin by discussing the role of this amygdala-mPFC circuitry in the conditioning and extinction of aversive learning in animals. We will then relate these data to emotional regulation paradigms in humans. Finally, we will consider how these processes are compromised in normal and pathological anxiety. We conclude that the capacity for efficient crosstalk between the amygdala and the mPFC, which is represented as the strength of the amygdala-mPFC circuitry, is crucial to beneficial outcomes in terms of reported anxiety.
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The dominant neurobiological model of anxiety disorders proposes that amygdala hyperreactivity corresponds to heightened emotional reactivity, while disrupted prefrontal processing corresponds to impaired emotion regulation.
“The prevailing neurobiological model of anxiety disorders posits that amygdala hyperreactivity to fearful or threatening stimuli is associated with heightened emotional reactivity, while disrupted processing in prefrontal regions is linked to impairments in emotional regulation (Berkman and Lieberman, 2009; Freitas-Ferrari et al., 2010; Kim et al., 2011).”
From Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry (2017) · cites this paper as Kim et al., 2011
Earlier research has shown that people with social anxiety disorder have heightened amygdala reactivity and altered prefrontal responses to social cues.
“Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD (Kim et al., 2011).”
From Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry (2017) · cites this paper as Kim et al., 2011
At the neurobiological level, social anxiety disorder involves disrupted activity in the neural circuitry for emotion regulation.
“Social anxiety disorder (SAD) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry.”
From Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry (2017) · cites this paper as Kim et al., 2011
Compared with healthy individuals, patients with social anxiety disorder show disrupted activation in the amygdala and prefrontal cortex.
“patients with SAD show: i) disrupted activation in the amygdala and regions of the prefrontal cortex (for reviews, see Berkman and Lieberman, 2009; Freitas-Ferrari et al., 2010; Kim et al., 2011)”
From Neural connectivity during affect labeling predicts treatment response to psychological therapies for social anxiety disorder. (2019) · cites this paper as Kim et al., 2011
Task fMRI work suggests vmPFC top-down regulation of amygdala, and amygdala-vmPFC coupling relates to trait anxiety in task and resting studies.
“task-based fMRI studies of emotion regulation suggest that the vmPFC is involved in top-down regulation of the amygdala, and functional coupling of the amygdala and vmPFC is related to trait anxiety in both task-related and resting-state studies13,14,15.”
From Developmental pathways to amygdala–prefrontal function and internalizing symptoms in adolescence (2012) · cites this paper as [13]
In non-human primates, monosynaptic projections from MPFC to basolateral amygdala inhibit activity in the central nucleus of the amygdala.
“Non-human primate research reveals a specific mechanism for these effects whereby monosynaptic input to basolateral amygdala from MPFC inhibits activity from the central nucleus of the amygdala (Kim et al., 2011).”
From Impact of short- and long-term mindfulness meditation training on amygdala reactivity to emotional stimuli (2018) · cites this paper as Kim et al., 2011
The amygdala facilitates responses to salient stimuli either positive or negative in valence and mediates emotional responses.
“The amygdala facilitates responses to salient stimuli either positive or negative in valence and mediates emotional responses (Kim et al., 2011).”
From Gaining insight into adolescent vulnerability for social anxiety from developmental cognitive neuroscience (2014) · cites this paper as Kim et al., 2011
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“As amygdala hyperactivation is a robust finding in anxiety disorders (Kim et al., 2011; Kolesar et al., 2019; Pantazatos et al., 2013), it is plausible that this initial anxiogen-esis is a result of increases in anxiety-related brain activation (Chavanne and Robinson, 2021; Fox and Shackman, 2019).”
Background
- Authors
- Kim, M. J., Loucks, R. A., Palmer, A. L., Brown, A. C., Solomon, K. M., Marchante, A. N., & Whalen, P. J.
- Affiliations
- Dartmouth College (US)
- Corresponding author
- Kim, M. Justin
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 223
- Issue
- 2
- Pages
- 403-410
- ISSN
- 0166-4328 (ISSN-L)
- PMC
- PMC3119771
- OpenAlex
- W2126054880
- Cited by
- 838
- References
- 132
- Citations by year
- 2026: 21 · 2025: 43 · 2024: 28 · 2023: 43 · 2022: 48 · 2021: 54 · 2020: 65 · 2019: 65 · 2018: 80 · 2017: 65 · 2016: 88 · 2015: 70 · 2014: 65 · 2013: 60 · 2012: 36
- FWCI
- 4.48
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (R01MH080716, F31MH090672)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Keywords
- amygdala, medial prefrontal cortex, anxiety, emotion regulation, fear conditioning, fear extinction, aversive learning, structural connectivity, functional connectivity
- MeSH terms
- Amygdala, Anxiety Disorders, Conditioning, Psychological, Emotions, Extinction, Psychological, Facial Expression, Fear, Humans, Magnetic Resonance Imaging, Neural Pathways, Social Environment, Stress Disorders, Post-Traumatic, Prefrontal Cortex
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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