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SUMMARY:STaR (Stress Timing affects Relapse): A model of the effects of st
 ress/glucocorticoids on extinction and relapse  - Dr Shira Meir Drexler - 
 Department of Cognitive Psychology Ruhr-University Bochum Germany
DTSTART:20190708T120000Z
DTEND:20190708T130000Z
UID:TALK126715@talks.cam.ac.uk
CONTACT:Lorraine Coulson
DESCRIPTION:Extinction learning is the most important underlying mechanism
  of exposure therapy\, a cognitive-behavioral psychotherapy commonly used 
 for the treatment of posttraumatic stress disorder and anxiety disorders. 
 Extinction creates a new inhibitory memory\, which presumably does not aff
 ect the original (e.g.\, fear) memory\; therefore\, relapse (e.g.\, return
  of fear) might occur after treatment. In recent years\, various research 
 groups aimed to augment extinction learning by the use of pharmacological 
 adjuvants\, e.g.\, the glucocorticoid (GC) stress hormone cortisol. Howeve
 r\, the role of timing of treatment on relapse has remained unclear until 
 lately. Based on recent works from our lab and additional groups\, in this
  talk I will introduce the StaR (Stress Timing affects Relapse) model\, a 
 theoretical model of the time-dependent effects of stress/GCs on extinctio
 n memory and relapse. In particular\, our findings show that (1) pre-extin
 ction stress/GCs promote memory consolidation in a context-independent man
 ner\, making extinction memory more resistant to relapse following context
  change. (2) Post-extinction stress also enhances the consolidation of ext
 inction\, but in a context-bound manner. These differences may result from
  the timing dependent effects of cortisol on emotional memory contextualiz
 ation. At the neural level\, the facilitation of extinction is reflected i
 n alterations in the amygdala-hippocampal-prefrontal cortex network. (3) S
 tress/GCs exposure before retrieval impairs extinction recall and promotes
  relapse. This may result from the stress-induced strengthening of amygdal
 a activation\, or disruption of the prefrontal cortex inhibitory functioni
 ng and its communication with additional brain regions that are crucial fo
 r extinction recall. I then discuss how the STaR model can contribute to t
 he understanding and prevention of relapse processes.
LOCATION:Kenneth Craik Room\, Craik Marshall Building\, Downing Site\, Cam
 bridge
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