Abstract:
OBJECTIVE: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. METHOD: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. RESULTS: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. CONCLUSION: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.
journal_name
Psychoneuroendocrinologyjournal_title
Psychoneuroendocrinologyauthors
Zuj DV,Palmer MA,Malhi GS,Bryant RA,Felmingham KLdoi
10.1016/j.psyneuen.2017.01.012subject
Has Abstractpub_date
2017-04-01 00:00:00pages
14-21eissn
0306-4530issn
1873-3360pii
S0306-4530(16)30764-8journal_volume
78pub_type
杂志文章abstract::We have studied the effects of ketanserin, a specific 5-HT2 antagonist, and zimelidine, a selective inhibitor of 5-HT re-uptake into central nervous system presynaptic terminals, upon basal and TRH stimulated serum TSH and prolactin levels in euthyroid individuals. Ten normal volunteers were studied (five male and fiv...
journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
doi:10.1016/0306-4530(84)90017-9
更新日期:1984-01-01 00:00:00
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pub_type: 杂志文章
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journal_title:Psychoneuroendocrinology
pub_type: 临床试验,杂志文章
doi:10.1016/s0306-4530(99)00061-x
更新日期:2000-04-01 00:00:00
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abstract::Using the learned helplessness model of depression in rats, the present study undertook to investigate the possibility of an impaired response to antidepressant drugs in diabetic animals. Experimental diabetes was induced by three intraperitoneal (IP) injections of streptozotocin (37.5, 37.5, 50 mg/kg, three days apar...
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journal_title:Psychoneuroendocrinology
pub_type: 临床试验,杂志文章
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
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journal_title:Psychoneuroendocrinology
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journal_title:Psychoneuroendocrinology
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journal_title:Psychoneuroendocrinology
pub_type: 临床试验,杂志文章
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pub_type: 杂志文章
doi:10.1016/j.psyneuen.2016.02.010
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journal_title:Psychoneuroendocrinology
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journal_title:Psychoneuroendocrinology
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journal_title:Psychoneuroendocrinology
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章,随机对照试验
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journal_title:Psychoneuroendocrinology
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doi:10.1016/j.psyneuen.2013.09.017
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pub_type: 杂志文章,评审
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
doi:10.1016/j.psyneuen.2012.07.009
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
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更新日期:2013-07-01 00:00:00
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journal_title:Psychoneuroendocrinology
pub_type: 杂志文章
doi:10.1016/j.psyneuen.2012.05.011
更新日期:2013-01-01 00:00:00
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journal_title:Psychoneuroendocrinology
pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:1998-05-01 00:00:00