How stress and glucocorticoids timing-dependently affect extinction and relapse

Drexler, Shira Meir; Merz, Christian J.; Jentsch, Valerie L.; Wolf, Oliver T.

doi:10.1016/j.neubiorev.2018.12.029

Cited by 45 publications

(31 citation statements)

References 116 publications

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“…As these findings demonstrate, one has to bear in mind that a given behavioral or pharmacological manipulation can lead to different behavioral outcomes when paired with either extinction (e.g., less fear: Meir Drexler et al, 2019a) or reconsolidation (e.g., more fear, at least in men: Meir Drexler et al, 2015). Unlike cortisol, more promising targets for future reconsolidation-based therapies may include the GC receptor antagonist mifepristone (Nikzad et al, 2011;Pitman et al, 2011), the noradrenergic β-blocker propranolol (Soeter and Kindt, 2015), or cognitive techniques for memory updating (Josselyn and Tonegawa, 2020;Wolf, 2017b, 2018), but more evidence in clinical populations is needed.…”

Section: Cortisol and Memory Reconsolidationmentioning

confidence: 99%

“…Recently, we suggested the STaR model (the initials of which stand for "Stress Timing affects Relapse"; see Figure 2) to illustrate the consequences of stress timing on the strength and context dependency of extinction memories, resulting in either relapse or not (Meir Drexler et al, 2019a). These findings are based on several studies in which we used exposure to laboratory stress or a pharmacological cortisol administration at different times: before extinction learning (i.e., to affect the encoding and consolidation of the extinction memory), after extinction learning (i.e., to affect extinction memory consolidation only), or before extinction retrieval.…”

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

“…At the neural level (as illustrated in Figure 3), we could show that the timing-dependent effects of stress/cortisol on extinction memories are modulated by alterations in the amygdala, the hippocampal complex, the prefrontal cortex, and their communication with other brain regions (Meir Drexler et al, 2019a). In line with evidence from previous works on animals and humans (Milad and Quirk, 2012), our findings suggest that the ventromedial prefrontal cortex (vmPFC) and the hippocampus are activated and determine, based on the given context, whether or not extinction memory is expressed under nonstressful conditions.…”

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

“…In contrast, stress or GCs before an extinction retrieval test impair extinction retrieval and promote relapse. Reprinted from Meir Drexler et al (2019a), Copyright (2019), with permission from Elsevier.…”

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

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Stress modulation of fear and extinction in psychopathology and treatment

et al. 2020

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The glucocorticoid cortisol, a major player in the development of stress-related psychopathology, can also be used for the augmentation of extinction-based psychotherapies (e.g., exposure therapy). Substantial evidence supports its beneficial effects in the treatment of post-traumatic stress disorder and specific phobias. In this review, we first present the role of stress and cortisol in the development of maladaptive emotional memories. Then, we describe the mechanisms that may account for the cortisol-induced augmentation of exposure, namely, the enhancement of extinction memory consolidation and the reduction of the contextual dependency of the extinction memory. Finally, we discuss several considerations and limitations for the use of cortisol in psychotherapy, focusing on the possible adverse effects of cortisol in a reconsolidation-based (as opposed to extinction-based) intervention.

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Section: Cortisol and Memory Reconsolidationmentioning

confidence: 99%

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

Section: Exposure Therapy and The Problem Of Relapsementioning

confidence: 99%

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Stress modulation of fear and extinction in psychopathology and treatment

et al. 2020

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“…The core reason for its ineffectiveness is an inability for the fear memory to be extinguished or at least not completely extinguished after exposure therapy. In addition to exposure therapy, drugassisted therapy is also needed to accelerate the extinction of fear memory [11].…”

Section: Introductionmentioning

confidence: 99%

Curculigoside facilitates fear extinction and prevents depression-like behaviors in a mouse learned helplessness model through increasing hippocampal BDNF

et al. 2019

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Curculigoside (CUR) is the main active component of traditional Chinese medicine Curculigoorchioides Gaertn (Xianmao in Chinese), which exhibits a variety of pharmacological activities. In this study we investigated the effects of CUR on fear extinction and related depression-like behaviors in mice. In fear conditioning task, we found that administration of CUR (1.6, 8, 40 mg•kg −1 •d −1 , ip, for 7 days) did not affect memory consolidation, but CUR at higher doses (8, 40 mg•kg −1 •d −1) significantly facilitated fear extinction, especially on D3 and D4. Moreover, CUR administration significantly ameliorated the fear conditioning-induced depression-like behaviors, likely through promoting fear extinction. We showed that CUR increased the expression of brain-derived neurotrophic factor (BDNF) and phosphorylation of tropomyosin receptor kinase B (TrkB) in the hippocampus, and activated protein kinase B (Akt)mammalian target of the rapamycin (mTOR) signaling pathway. Administration of the selective TrkB agonist 7,8-dihydroxyflavone (7,8-DHF, 5 mg•kg −1 •d −1 , ip) also facilitated fear extinction, ameliorated depression-like behaviors. We established a mouse learned helplessness (LH) model to evaluate the antidepressant activity of CUR. The spatial memory was assessed in Morris water maze. We showed that LH-induced depression-like behaviors, including prolonged immobility times in forced swim and tail suspension tests as well as spatial memory impairments; LH also downregulated BDNF expression and the Akt-mTOR signaling pathway in the hippocampus. Administration of CUR (1.6, 8, 40 mg•kg −1 •d −1 , ip, for 14 days) or 7,8-DHF (5 mg•kg −1 •d −1 , ip, for 3 days) prevented LH-induced depression-like behaviors and promoted BDNF expression and the Akt-mTOR signaling pathway. In conclusion, CUR can accelerate the fear memory extinction and ameliorate depression-like behaviors in mice via promoting BDNF expression and activating the Akt-mTOR signaling pathway in the hippocampus.

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How Different Factors in Combination Change Fear Extinction Learning: The Case of Sex and Stress Hormones

Merz

2023

Fear Extinction

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How stress and glucocorticoids timing-dependently affect extinction and relapse

Cited by 45 publications

References 116 publications

Stress modulation of fear and extinction in psychopathology and treatment

Stress modulation of fear and extinction in psychopathology and treatment

Curculigoside facilitates fear extinction and prevents depression-like behaviors in a mouse learned helplessness model through increasing hippocampal BDNF

How Different Factors in Combination Change Fear Extinction Learning: The Case of Sex and Stress Hormones

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