STRESS SENSITIZATION AND FEAR LEARNING IN POSTTRAUMATIC STRESS DISORDER

2007 ◽  
Vol 44 (s1) ◽  
pp. S8-S9 ◽  
2010 ◽  
Vol 35 (6) ◽  
pp. 1402-1411 ◽  
Author(s):  
Igor Ponomarev ◽  
Vinuta Rau ◽  
Edmond I Eger ◽  
R Adron Harris ◽  
Michael S Fanselow

2018 ◽  
Author(s):  
Marissa Elizabeth Maheu ◽  
Joseph Hunter Howie ◽  
Kerry James Ressler

Posttraumatic stress disorder (PTSD) and acute stress disorder are precipitated by exposure to one or more traumatic events, and result in debilitating fear-related symptoms. Advances made over the past several years have greatly improved our understanding of these disorders, as well as the neurobiological and genetic factors that contribute to their emergence and progression. In this review, we provide an overview of this research, with a particular focus on recent developments in understanding the neurocircuitry underlying relevant aspects of fear learning, including acquisition, generalization, and the extinction of fear. Molecular regulators of stress response and candidate genes implicated in PTSD are also discussed. Although there remains a great deal to learn about these disorders, novel approaches, large-scale genomic studies, and new molecular techniques promise to help untangle the neurobiology of trauma- and stressor-related illness over the coming years. This review contains 3 figures, 3 tables and 56 references Key words: Posttraumatic stress disorder, fear, genetics, GWAS, HPA stress response, neurocircuitry models of trauma, generalization, extinction learning.


2016 ◽  
Vol 17 (12) ◽  
pp. 1325-1333 ◽  
Author(s):  
Josef Jenewein ◽  
Jeannine Erni ◽  
Hanspeter Moergeli ◽  
Christian Grillon ◽  
Sonja Schumacher ◽  
...  

Author(s):  
Christine Heim ◽  
Katharina Schultebraucks ◽  
Charles R. Marmar ◽  
Charles B. Nemeroff

This chapter examines current findings relating to the molecular neuropharmacology of posttraumatic stress disorder (PTSD). Studies consistently show that neurochemical alterations after trauma exposure are associated with the development of PTSD and reflect in part stress sensitization in PTSD. We also review neuroendocrine, neurotransmitter, neuropeptide, and related molecular features that reflect preexisting vulnerability factors for the development of PTSD. In this chapter, we provide an overview of recent neuroendocrine findings mainly with regard to the influence of the hypothalamic-pituitary-axis. We also review recent neurochemical findings including the influence of different neurotransmitters such as catecholamines, serotonin, amino acids, neuropeptides, neurotrophins, and lipids. We incorporate these new and established neurobiological findings into a proposed integrative model of the neurobiology of PTSD.


2015 ◽  
Vol 5 (12) ◽  
pp. e700-e700 ◽  
Author(s):  
R A Morey ◽  
◽  
J E Dunsmoor ◽  
C C Haswell ◽  
V M Brown ◽  
...  

2021 ◽  
Author(s):  
Allison Letkiewicz ◽  
Amy L. Cochran ◽  
Anthony Privatsky ◽  
G. Andrew James ◽  
Josh M. Cisler

Learning theories of posttraumatic stress disorder (PTSD) purport that fear learning processes, such as those that support fear acquisition and extinction, are impaired. Computational models that aim to capture specific processes involved in fear learning have primarily assessed model free, or trial-and-error, reinforcement learning (RL). Although prior research indicates that aspects of model-free RL are disrupted among individuals with PTSD, models have yet to quantify and identify whether more nuanced, contextually driven learning is also disrupted. Given empirical evidence of aberrant contextual modulation of fear in PTSD, the present study sought to identify whether model-based RL processes are altered during fear conditioning among women with interpersonal violence (IPV)-related PTSD (n=85) using computational modeling. Several traditional models and a latent-state model that captured model-based RL were applied to skin conductance responses (SCR) collected during fear acquisition and extinction, and the latent-state model was identified as the best fitting model. Model-derived parameters from the latent-state model were carried forward to neuroimaging analyses (voxel-wise and independent component analysis) and results revealed that reduced latent-state related activity within visual processing regions uniquely predicted higher PTSD symptoms. Additionally, after controlling for latent-state update-related encoding, greater value estimation encoding within the left frontoparietal network during fear acquisition and reduced value estimation encoding within the dorsomedial prefrontal cortex during fear extinction predicted greater PTSD symptoms. Results provide evidence of disrupted model-based RL processes in women with IPV-related PTSD, which may contribute to difficulties revising fear and safety information. Future work should further assess model-based RL in PTSD.


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