Circuits and systems in stress. II. Applications to neurobiology and treatment in posttraumatic stress disorder
Abstract
This paper follows the preclinical work on the effects of stress on neurobiological and neuroendocrine systems and provides a comprehensive working model for understanding the pathophysiology of posttraumatic stress disorder (PTSD). Studies of the neurobiology of PTSD in clinical populations are reviewed. Specific brain areas that play an important role in a variety of types of memory are also preferentially affected by stress, including hippocampus, amygdala, medial prefrontal cortex, and cingulate. This review indicates the involvement of these brain systems in the stress response, and in learning and memory. Affected systems in the neural circuitry of PTSD are reviewed (hypothalamic-pituitary-adrenal axis (HPA-axis), catecholaminergic and serotonergic systems, endogenous benzodiazepines, neuropeptides, hypothalamic-pituitary-thyroid axis (HPT-axis), and neuro-immunological alterations) as well as changes found with structural and functional neuroimaging methods. Converging evidence has emphasized the role of early-life trauma in the development of PTSD and other trauma-related disorders. Current and new targets for systems that play a role in the neural circuitry of PTSD are discussed. This material provides a basis for understanding the psychopathology of stress-related disorders, in particular PTSD.
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Ongoing impairment of PFC functioning causes chronic reduction in descending inhibitory influences from PFC on brainstem nuclei and amygdala, which could underlie PTSD symptoms such as chronic hypervigilance, attention deficits, and impaired executive functioning.
“The ongoing impairment of PFC functioning would result in a chronic reduction in descending inhibitory influences from the PFC on brainstem nuclei and the amygdala (Williams et al. [405]), which could form the basis of certain symptoms of PTSD, such as chronic hypervigilance, attention deficits, and impaired executive functioning (Vermetten and Bremner [406]; Shin et al. [407]; Britton et al. [408”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Vermetten and Bremner [406]
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- Authors
- Vermetten, E., & Bremner, J. D.
- Affiliations
- Emory University (US)
- Corresponding author
- Vermetten, Eric
- Venue
- Depression and Anxiety
- Publisher
- Hindawi Limited
- Published
- 2002
- Volume
- 16
- Issue
- 1
- Pages
- 14-38
- ISSN
- 1091-4269 (ISSN-L)
- 1520-6394
- OpenAlex
- W2133070502
- Cited by
- 210
- References
- 21
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 8 · 2019: 6 · 2018: 5 · 2017: 4 · 2016: 18 · 2015: 6 · 2014: 7 · 2013: 11 · 2012: 8
- FWCI
- 1.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Depression and Anxiety (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- post-traumatic stress disorder, stress response, neuroendocrine system, hypothalamic-pituitary-adrenal axis, catecholaminergic system, serotonergic system, neuropeptides, hypothalamic-pituitary-thyroid axis, hippocampus, amygdala, medial prefrontal cortex, cingulate cortex, memory, early trauma, neural circuits, neuroimaging, PTSD treatment
- MeSH terms
- Animals, Arousal, Brain, Brain Mapping, Humans, Nerve Net, Stress Disorders, Post-Traumatic, Receptors, Neurotransmitter, Neurotransmitter Agents
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