Cold pressor test improves fear extinction in healthy men

Antov, Martin I.; Melicherová, Ursula; Stockhorst, Ursula

doi:10.1016/j.psyneuen.2015.01.009

Cited by 18 publications

(11 citation statements)

References 24 publications

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“…Experimental studies investigating underlying mechanisms of anxiety disorders and their treatment often use classical fear conditioning and extinction paradigms (Antov, Melicherov a, & Stockhorst, 2015;Britton, Evans, & Hernandez, 2014;Duits et al, 2015;Lissek et al, 2008;Wang et al, 2015). After pairing a conditioned stimulus (CS) with an aversive unconditioned stimulus (US) during a conditioning procedure, the CS elicits a conditioned response (CR), which is similar to the spontaneous reaction (unconditioned response, UR) that typically follows the US (LeDoux, 2000).…”

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confidence: 99%

A pragmatic comparison of noise burst and electric shock unconditioned stimuli for fear conditioning research with many trials

et al. 2016

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Several methods that are promising for studying the neurophysiology of fear conditioning (e.g., EEG, MEG) require a high number of trials to achieve an adequate signal‐to‐noise ratio. While electric shock and white noise burst are among the most commonly used unconditioned stimuli (US) in conventional fear conditioning studies with few trials, it is unknown whether these stimuli are equally well suited for paradigms with many trials. Here, N = 32 participants underwent a 260‐trial differential fear conditioning and extinction paradigm with a 240‐trial recall test 24 h later and neutral faces as conditioned stimuli. In a between‐subjects design, either white noise bursts (n = 16) or electric shocks (n = 16) served as US, and intensities were determined using the most common procedure for each US (i.e., a fixed 95 dB noise burst and a work‐up procedure for electric shocks, respectively). In addition to differing US types, groups also differed in closely linked US‐associated characteristics (e.g., calibration methods, stimulus intensities, timing). Subjective ratings (arousal/valence), skin conductance, and evoked heart period changes (i.e., fear bradycardia) indicated more reliable, extinction‐resistant, and stable conditioning in the white noise burst versus electric shock group. In fear conditioning experiments where many trials are presented, white noise burst should serve as US.

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confidence: 99%

A pragmatic comparison of noise burst and electric shock unconditioned stimuli for fear conditioning research with many trials

et al. 2016

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“…The findings of the current study suggest that noradrenergic activity may not be a moderating factor of immediate extinction learning, however increased noradrenergic signaling is known to enhance emotional learning and memory processes (Mueller and Cahill, 2010). Previous research has used behavioral (e.g., Antov et al, 2015;Antov et al, 2013) and pharmacological tasks (e.g., Soeter and Kindt, 2012) designed to activate the stress response and subsequent catecholamine release. The current study involved the collection of endogenous sAA levels prior to and immediately following fear acquisition.…”

Section: Discussionmentioning

confidence: 60%

“…While the US (in this case, a mild electric shock) appeared to increase sAA release, these levels showed no interaction with group or fear extinction learning ability. Previous research showing clear links between NA (or sympathetic arousal) and fear extinction directly 20 manipulated noradrenergic signaling either through pharmacological intervention or via stress-induction tasks (Antov et al, 2015). These research design differences may have led to greater changes in NA, compared to changes seen in the current study.…”

Section: Discussionmentioning

confidence: 77%

“…Alternatively, rodent studies show that yohimbine is associated with context-and dose-dependent enhancements in fear extinction when administered immediately prior to extinction (Cain et al, 2004;Morris and Bouton, 2007). Behavioral research in humans shows that strategically timed stress induction tasks (and associated increases in sympathetic arousal) have the capacity to strengthen fear acquisition (Antov et al, 2013), and enhance fear extinction (Antov et al, 2015), when the stress task is performed immediately prior to the respective acquisition/extinction phase. Mueller and Cahill (2010) argue that NA modulation on extinction is strongest when the relationship between the conditioned stimulus (CS) and the unconditioned stimulus (US) is most predictable.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, we were interested in the role of sAA in response to fear conditioning as a moderator between fear extinction learning ability and PTSD symptom severity in a sample with current PTSD, trauma exposure without PTSD, and non-trauma-exposed controls. Based on recent research using sAA as an indicator of NA in intrusive memories (Bryant et al, 2013;Nicholson et al, 2014), and the role of noradrenergic signaling in fear conditioning and extinction (Antov et al, 2015;Antov and Stockhorst, 2014;Soeter and Kindt, 2012), we predicted that sAA levels would moderate the relationship between fear extinction learning and PTSD symptoms. Specifically, we hypothesized that poorer fear extinction learning ability would be associated with greater PTSD symptom severity, and that this relationship would be stronger with lower sAA levels in response to fear conditioning.…”

Section: Introductionmentioning

confidence: 99%

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Endogenous salivary α-amylase does not interact with skin conductance response during fear extinction in posttraumatic stress disorder

Zuj

Palmer

Malhi

et al. 2018

Psychiatry Research

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Posttraumatic Stress Disorder (PTSD) is associated with elevated noradrenergic signaling, which has an impact on emotional learning and memory. Fear extinction is thought to underlie the processes of exposure therapy, however the relationship between noradrenaline and extinction in PTSD is unclear. Participants with PTSD (n = 21), trauma-exposure without PTSD (TC; n = 36), and non-trauma-exposed controls (NTC; n = 27) completed a fear conditioning and extinction paradigm, and conditioned fear was indexed by skin conductance response (SCR). Salivary α-amylase (sAA) collected at baseline and immediately post-fear acquisition was used as an index of noradrenaline, and we examined whether sAA in response to fear acquisition was a moderator between fear extinction and PTSD symptoms. While there was a significant increase in sAA from baseline to post-fear acquisition, this was not modulated by group. Compared to TC and NTC, the PTSD group displayed a slower decline in SCRs during early extinction, which generalized across stimulus type, and was not moderated by sAA. These findings suggest that the relationship between fear extinction and PTSD symptoms does not change as a function of sAA levels; however previous research suggests other processes of fear learning may be associated with noradrenergic activity in PTSD.

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