It has been more than a decade since Ressler et al. published the first demonstration of facilitation of exposure-based therapy with
the N-methyl-D-aspartate co-agonist D-cycloserine (
1
). Since that pivotal study, there has been a surge of research to identify additional
targets that enhance fear extinction for adjunctive treatment strategies. Potential
pathways include catecholamines, endocannabinoids, and various neuropeptide systems
and epigenetic pathways (
1
). Among the neuropeptide candidates, oxytocin (OT) has gained attention as a modulator
of conditioned fear processes including fear extinction. OT receptors are located
on neural circuits mediating fear learning and extinction, and there is substantial
preclinical literature supporting modulatory effects of OT receptor signaling on conditioned
fear learning, recall, and extinction (
2
). Furthermore, the putative prosocial effects of OT make it attractive as an adjunctive
treatment for behavioral therapies, as it may facilitate patient-therapist alliance
and acceptability of treatment. Initial support for the hypothesis that OT may enhance
fear extinction in humans came from a study from our laboratory, which found that
OT administration before extinction training significantly increased 24-hour extinction
recall. However, the mechanism by which OT affects extinction in humans is unknown.To read this article in full you will need to make a payment
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References
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Article info
Publication history
Accepted:
June 2,
2015
Received:
June 1,
2015
Identification
Copyright
Published by Elsevier Inc.
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Access this article on ScienceDirectLinked Article
- Oxytocin Facilitates the Extinction of Conditioned Fear in HumansBiological PsychiatryVol. 78Issue 3
- PreviewCurrent neurocircuitry models of anxiety disorders posit a lack of inhibitory tone in the amygdala during acquisition of Pavlovian fear responses and deficient encoding of extinction responses in amygdala–medial prefrontal cortex circuits. Competition between these two responses often results in a return of fear, limiting control over anxiety. However, one hypothesis holds that a pharmacologic strategy aimed at reducing amygdala activity while simultaneously augmenting medial prefrontal cortex function could facilitate the extinction of conditioned fear.
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