Lower estradiol predicts increased reinstatement of fear in women.

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Publisher: Elsevier Science Publishers
Document Type: Report; Brief article
Length: 356 words

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Keywords Fear reinstatement; Estradiol; Sex hormones; Return of fear; Relapse of fear Highlights * Estradiol is implicated in fear extinction recall . * No human studies have examined the influence of estradiol on fear reinstatement . * Lower estradiol predicted increased fear reinstatement in women. * Progesterone did not predict significant differences in fear reinstatement. * Estradiol may be important in protecting against the return of fear. Abstract Low levels of estradiol in women have been associated with impaired fear extinction recall, with suggestions this may promote the return of fear and heighten the female vulnerability for anxiety disorders. A particularly important measure for the return of fear is reinstatement, but no human studies to date have examined the impact of estradiol on fear reinstatement. Forty-two healthy females completed a differential fear conditioning, extinction and reinstatement task with skin conductance response (SCR) amplitude indexing level of conditioned fear. Saliva samples were taken to measure estradiol and progesterone. To examine fear reinstatement, SCR amplitude was compared between the last trial of the late extinction phase to the first re-extinction trial following the unsignaled presentation of two aversive electric shocks. No significant effects of estradiol were found for acquisition of fear conditioning or fear extinction learning. Lower estradiol predicted a significantly larger generalized SCR amplitude at re-extinction (post-reinstatement) in women. This provides novel evidence suggesting a protective role of estradiol in potentially reducing the relapse of fear following re-exposure to aversive stimuli, although further research is necessary in clinical populations to clarify this effect. Author Affiliation: (a) School of Psychological Sciences, University of Melbourne, Australia (b) Division of Psychology, School of Medicine, University of Tasmania, Australia (c) Department of Psychology, Swansea University, UK (d) School of Psychology, University of New South Wales, Australia * Corresponding author. School of Psychological Sciences, The University of Melbourne, VIC, 3010, Australia. Article History: Received 14 April 2018; Revised 7 October 2020; Accepted 19 April 2021 Byline: Kim L. Felmingham [kfelmingham@unimelb.edu.au] (a,*), Julia M. Caruana (a), Lisa N. Miller (a), Luke J. Ney (b), Daniel V. Zuj (b,c), Chia Ming K. Hsu (b), Emma Nicholson (b), Annie To (b), Richard A. Bryant (d)

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Gale Document Number: GALE|A664259800