title: Endogenous cortisol reactivity moderates the relationship between fear inhibition to safety signals and posttraumatic stress disorder symptoms.
abstract: Posttraumatic stress symptoms (PTSS) are commonly associated with impairments in extinguishing fear to signals previously associated with danger, and also with inhibiting fear to safety signals. Previous studies indicate that PTSS are associated with low cortisol activity, and cortisol is shown to facilitate fear extinction. Few studies have examined the influence of cortisol reactivity on fear extinction in PTSS.
  
  
  
  We used a standardized fear conditioning and extinction paradigm to investigate the relationship between fear extinction and endogenous salivary cortisol activity in participants with high PTSS (n=18), trauma-exposed controls (n=33), and non-trauma-exposed controls (n=27). Skin conductance response (SCR) was used as an index of conditioned responding. Saliva samples were collected at baseline, and 20min post-fear acquisition for basal and reactive cortisol levels, respectively.
  
  
  
  PTSS participants demonstrated a slower rate of extinction learning during the early extinction phase. A moderation analysis revealed that cortisol reactivity was a significant moderator between fear inhibition to the safety signal (CS-) during early extinction and PTSS, but not to the threat signal (CS+). Specifically, this interaction was significant in two ways: (1) participants with elevated cortisol reactivity showed lower PTSS as fear inhibition improved; and (2) participants with low cortisol reactivity showed higher PTSS as fear inhibition improved.
  
  
  
  The findings of the present study show that the relationship between fear inhibition and cortisol reactivity is complex, and suggest that cortisol reactivity shapes safety signal learning in PTSS.
authors.affiliation: Division of Psychology, School of Medicine, University of Tasmania, Australia. Electronic address: Daniel.Zuj@utas.edu.au.
authors.forename: Daniel V
authors.initials: DV
authors.lastname: Zuj
authors.affiliation: Division of Psychology, School of Medicine, University of Tasmania, Australia.
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Palmer
authors.affiliation: Royal North Shore Hospital, Sydney, Australia; Sydney Medical School, University of Sydney, Australia.
authors.forename: Gin S
authors.initials: GS
authors.lastname: Malhi
authors.affiliation: School of Psychology, University of New South Wales, Australia.
authors.forename: Richard A
authors.initials: RA
authors.lastname: Bryant
authors.affiliation: School of Psychological Sciences, University of Melbourne, Australia.
authors.forename: Kim L
authors.initials: KL
authors.lastname: Felmingham
mesh_terms: D000293:Adolescent; D000328:Adult; D003214:Conditioning, Classical / Q000502:physiology*; D005108:Extinction, Psychological / Q000502:physiology*; D005239:Fear / Q000502:physiology*; D005260:Female; D005712:Galvanic Skin Response / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012463:Saliva / Q000737:chemistry; D013313:Stress Disorders, Post-Traumatic / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D006854:Hydrocortisone
keywords: Cortisol; Fear extinction; Fear inhibition; HPA axis; Posttraumatic stress disorder