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Systematic investigation of the experimental boundary conditions and mechanisms contributing to reinstatement of fear in humans.

Subject Area Biological Psychiatry
Human Cognitive and Systems Neuroscience
Term from 2014 to 2019
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 258608397
 
Relapse after successful psychological or pharmacological treatment represents a major problem in the treatment of anxiety patients. Relapse, or in other words, return of fear (ROF), can be triggered by the mere passage of time (spontaneous recovery), induction of contextual change (renewal) or by exposure to unsignaled USs (reinstatement). Reinstatement has been described in rodents decades ago, but human research has just begun. In the recent years a continuous increases in the use of reinstatement has been observed e.g as the critical outcome test in fear conditioning studies investigating long-term recall in the reconsolidation literature. More specifically, out of twenty reinstatement studies published to date in humans, only eight have been published before the year 2012. A major problem here is that experimental details, data analyses and consequently results vary widely as no systematic investigation of the experimental boundary conditions and mechanisms contributing to reinstatement in humans have been conducted to date. It thus remains unclear whether the results of the early rodent work can be translated to humans. As this renders comparisons and interpretation of the findings difficult to date, this project aims at 1) establishing these experimental, in particular contextual, boundary conditions contributing to reinstatement in humans 2) exploring the mechanisms (e.g. mediated conditioning, context conditioning, non-associative processes) and 3) exploring the neural underpinnings mediating reinstatement in humans. The results of this project might contribute to the understanding of divergent previous findings (e.g. differential vs. generalized reinstatement) and pave the way to a more standardized experimental approach. Having established this will finally allow us to systematically investigate individual and biological differences (e.g. through pharmacological interventions or genetic polymorphisms) in reinstatement. Ultimately, a better understanding of the circumstances facilitating or attenuating reinstatement in experimental protocols may aid our understanding of clinical relapse and thus might ultimately help to improve cognitive-behavioural treatment procedures.
DFG Programme Research Grants
 
 

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