The Influence of Stress Hormones on Fear Circuitry
Abstract
Fear arousal, initiated by an environmental threat, leads to activation of the stress response, a state of alarm that promotes an array of autonomic and endocrine changes designed to aid self-preservation. The stress response includes the release of glucocorticoids from the adrenal cortex and catecholamines from the adrenal medulla and sympathetic nerves. These stress hormones, in turn, provide feedback to the brain and influence neural structures that control emotion and cognition. To illustrate this influence, we focus on how it impacts fear conditioning, a behavioral paradigm widely used to study the neural mechanisms underlying the acquisition, expression, consolidation, reconsolidation, and extinction of emotional memories. We also discuss how stress and the endocrine mediators of the stress response influence the morphological and electrophysiological properties of neurons in brain areas that are crucial for fear-conditioning processes, including the amygdala, hippocampus, and prefrontal cortex. The information in this review illuminates the behavioral and cellular events that underlie the feedforward and feedback networks that mediate states of fear and stress and their interaction in the brain.
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In animals, chronic stress results in prolonged release of glucocorticoids and leads to hypertrophy of the amygdala and nucleus accumbens, atrophy of the hippocampus and prefrontal cortex, and functional impairment of the PFC.
“In animals, chronic stress results in the prolonged release of glucocorticoids and leads to hypertrophy of the amygdala and nucleus accumbens, atrophy of the hippocampus and prefrontal cortex (PFC), and functional impairment of the PFC (44–55).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [46]
Glucocorticoid actions in the prefrontal cortex impair working memory and may indirectly exacerbate working memory impairments through interactions with catecholamine systems.
“While this release is critical to the enhancement of long term memories associated with the event (Rodrigues et al., 2009), glucocorticoid actions in the PFC impair working memory.”
From Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex (2013) · cites this paper as Rodrigues et al., 2009
Tasks that rely on the habitual functions of basal ganglia circuits or the emotional conditioning of the amygdala are spared or even enhanced by stress exposure.
“Later research in animals demonstrated that exposure to acute, uncontrollable stress impairs the working memory abilities of the PFC19,20, while tasks that rely on the habitual functions of basal ganglia circuits, for example20,21, or the emotional conditioning of the amygdala22 are spared or even enhanced by stress exposure (Fig. 1b).”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [22]
In contrast to that in PFC, high levels of catecholamines strengthen the affective responses of the amygdala, the habitual or compulsive responses of the striatum and sensory processing in the primary somatosensory cortex.
“In contrast to that in PFC, high levels of catecholamines strengthen the affective responses of the amygdala22,64, the habitual or compulsive responses of the striatum65 and sensory processing in the primary somatosensory cortex66.”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [22]
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“, Darwinian fitness), such as an effect on subsequent reproduction, must be maladaptive; and since the “function” of the stress axis is to maintain homeostasis, chronic stress must be pathological (Lupien et al., 2009; Rodrigues et al., 2009; Sheriff et al., 2009).”
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- Authors
- Rodrigues, S. M., LeDoux, J. E., & Sapolsky, R. M.
- Affiliations
- Oregon State University (US)
- New York University (US)
- Stanford Medicine (US)
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- Published
- 2009-06-01
- Volume
- 32
- Issue
- 1
- Pages
- 289-313
- ISSN
- 0147-006X (ISSN-L)
- 1545-4126
- OpenAlex
- W2151027504
- Cited by
- 556
- References
- 33
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 20 · 2023: 21 · 2022: 29 · 2021: 27 · 2020: 45 · 2019: 30 · 2018: 28 · 2017: 31 · 2016: 38 · 2015: 40 · 2014: 34 · 2013: 55 · 2012: 40
- FWCI
- 3.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG020633)
- National Institute of Mental Health (P50MH058911, K05MH067048, R01MH046516, R37 MH037884)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- stress hormones, fear conditioning, stress response, glucocorticoids, catecholamines, fear memory consolidation, fear memory reconsolidation, fear extinction, amygdala, hippocampus, prefrontal cortex, neuronal morphology, neuronal electrophysiology, emotional memory
- MeSH terms
- Animals, Brain, Catecholamines, Fear, Glucocorticoids, Hormones, Humans, Hypothalamo-Hypophyseal System, Neurosecretory Systems, Pituitary-Adrenal System, Stress, Psychological
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