Block of glucocorticoid synthesis during re-activation inhibits extinction of an established fear memory
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TLDR
It is demonstrated that extinction of a classical contextual fear memory is dependent on endogenous glucocorticoid synthesis during re-activation of a fear memory, thus contributing to one of the core symptoms of PTSD.About:
This article is published in Neurobiology of Learning and Memory.The article was published on 2011-05-01 and is currently open access. It has received 71 citations till now. The article focuses on the topics: Traumatic memories & Extinction (psychology).read more
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Stress, glucocorticoids and memory: implications for treating fear-related disorders
TL;DR: Important advances in the understanding of how glucocorticoid stress hormones mediate stress effects on memory processes are reviewed, and the translational potential of these new conceptual insights are discussed.
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Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders.
TL;DR: The current body of research reveals important new insights into the neurobiology and neurochemistry of fear extinction and holds significant promise for pharmacologically-augmented psychotherapy as an improved approach to treat trauma and anxiety-related disorders in a more efficient and persistent way promoting enhanced symptom remission and recovery.
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Stress and Fear Extinction.
Stephen Maren,Andrew Holmes +1 more
TL;DR: Emerging evidence that stress impairs recovery from trauma by impairing fear extinction is examined, a form of learning thought to underlie the suppression of trauma-related fear memories.
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Stress and glucocorticoid receptor-dependent mechanisms in long-term memory: from adaptive responses to psychopathologies.
TL;DR: The hypothesis that stress promotes the formation of strong long-term memories is proposed because the activation of hippocampal GRs after learning is coupled to the recruitment of the growth and pro-survival BDNF/cAMP response element-binding protein (CREB) pathway, which is well-know to be a general mechanism required for long- term memory formation.
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The hypothalamic-pituitary-adrenal axis in PTSD: Pathophysiology and treatment interventions.
Boadie W. Dunlop,Andrea Wong +1 more
TL;DR: Hydrocortisone given to prevent PTSD following a trauma is the best supported HPA axis intervention for PTSD, including the role of glucocorticoids as part of medication enhanced psychotherapy.
References
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Stress and the brain: from adaptation to disease
TL;DR: In response to stress, the brain activates several neuropeptide-secreting systems, which eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators as mentioned in this paper.
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Stress, memory and the amygdala
TL;DR: The unique features of stress-induced plasticity in the amygdala, in association with changes in other brain regions, could have long-term consequences for cognitive performance and pathological anxiety exhibited in people with affective disorders.