Electrodermal and subjective reactions to fear-relevant stimuli under threat of shock

Lovibond, Peter F.; Hanna, Sharon; Siddle, David A.T.; Bond, Nigel W.

doi:10.1080/00049539408259476

Cited by 15 publications

(13 citation statements)

References 32 publications

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“…Evidence from my laboratory supports an alternative view that fear-relevant stimuli have an innate prepotency to elicit fear responses that may be sensitized by appropriate environmental conditions such as a separate source of arousal or anxiety (Lovibond et al 1994; see also Menzies and Clarke 1995). According to this view, the apparent resistance to extinction of fear-relevant stimuli arises from selective sensitization of innate fear responses, superimposed on normal extinction of associative learning ).…”

Section: Laboratory Researchmentioning

confidence: 65%

Cognitive Processes in Extinction: Figure 1

Lovibond

2004

Learn. Mem.

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Human conditioning research shows that learning is closely related to consciously available contingency knowledge, requires attentional resources, and is influenced by language. This research suggests a cognitive model in which extinction consists of changes in contingency beliefs in long-term memory. Laboratory and clinical evidence on extinction is briefly reviewed, and it is concluded that the evidence supports the cognitive position. There is little evidence for a separate, noncognitive conditioning system. The primary implication for neural analysis is that learning and extinction are unlikely to be reducible to direct connections in which one stimulus simply activates or inhibits the memory representation of another. Rather, an adequate neural model will involve the integration of both low-level and high-level systems, including attention, representation of stimulus relations in long-term memory, and a dynamic performance mechanism based on anticipation, not just activation.Extinction refers to the loss of an associatively based behavior when the associative relationships that generated the original learning have been changed. For example, in Pavlovian conditioning, the conditioned response (CR) declines over trials when the conditioned stimulus (CS) is no longer followed by the unconditioned stimulus (US). The way in which we view extinction necessarily follows from the way in which we conceptualize the initial conditioning. Psychologists, neuroscientists, and lay people alike share a common conceptualization of conditioning: It is seen as an automatic, unconscious, and low-level process that establishes excitatory or inhibitory associations between CS and US nodes in memory. In humans, conditioning is almost universally agreed to involve separate mechanisms from those involved in reasoning, language, and consciousness. Accordingly, extinction is also seen as an automatic and unconscious process that either reverses the original learned associations, or establishes new competing associations. But what if this traditional view of conditioning and extinction is wrong?In fact, research on conditioning in humans suggests it to be an entirely different process from that suggested by the traditional view. Evidence for a separate conditioning mechanism that is independent of higher cognitive processes has been remarkably difficult to obtain (Brewer 1974;Dawson and Schell 1985;Lovibond and Shanks 2002). Instead, conditioning in humans appears to be closely tied to attention, consciousness, and language. In this article, I will briefly summarize this research, then focus specifically on extinction in human conditioning, and finally consider the implications for research into the neural basis of conditioning and extinction in both animals and humans.

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Section: Laboratory Researchmentioning

confidence: 65%

Cognitive Processes in Extinction: Figure 1

Lovibond

2004

Learn. Mem.

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110

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“…One of the fear-relevant stimuli (CS2) served as control for the other fear-relevant stimulus (CS1). However, since fear-relevant stimuli are known to have an innate prepotency to elicit fear responses (Lovibond et al, 1994), we employed an additional fear-irrelevant control stimulus (CS3) to verify whether the procedure was capable of neutralizing the acquired fear responding. Testing included several phases across three subsequent days, each separated by 24 h. During each session, participants sat behind a table with a computer monitor at a distance of 50 cm in a sound-attenuated room.…”

Section: Methodsmentioning

confidence: 99%

Stimulation of the Noradrenergic System during Memory Formation Impairs Extinction Learning but not the Disruption of Reconsolidation

Soeter

Kindt

2011

Neuropsychopharmacol

133

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The noradrenergic system plays a critical role in the 'consolidation' of emotional memory. If we are to target 'reconsolidation' in patients with anxiety disorders, the noradrenergic strengthening of fear memory should not impair the disruption of reconsolidation. In Experiment I, we addressed this issue using a differential fear conditioning procedure allowing selective reactivation of one of two fear associations. First, we strengthened fear memory by administering an α(2)-adrenergic receptor antagonist (ie, yohimbine HCl; double-blind placebo-controlled study) 30 min before acquisition (time for peak value yohimbine HCl <1 h). Next, the reconsolidation of one of the fear associations was manipulated by administering a β-adrenergic receptor antagonist (ie, propranolol HCl) 90 min before its selective reactivation (time for peak value propranolol HCl <2 h). In Experiment II, we administered propranolol HCl after reactivation of the memory to rule out a possible effect of the pharmacological manipulation on the memory retrieval itself. The excessive release of noradrenaline during memory formation not only delayed the process of extinction 48 h later, but also triggered broader fear generalization. Yet, the β-adrenergic receptor blocker during reconsolidation selectively 'neutralized' the fear-arousing aspects of the noradrenergic-strengthened memory and undermined the generalization of fear. We observed a similar reduction in fear responding when propranolol HCl was administered after reactivation of the memory. The present findings demonstrate the involvement of noradrenergic modulation in the formation as well as generalization of human fear memory. Given that the noradrenergic strengthening of fear memory impaired extinction learning but not the disruption of reconsolidation, our findings may have implications for the treatment of anxiety disorders.

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“…One of the fear-relevant stimuli (CS2) served as control for the other fear-relevant stimulus (CS1). However, as fear-relevant stimuli are known to have an innate prepotency to elicit fear responses (Lovibond et al 1994), we employed an additional fear-irrelevant control cue (CS3) to verify whether the procedure was capable of neutralizing fear responding. In Experiment I, all of the participants received single-blind an oral dose of 40 mg of propranolol, a b-adrenergic receptor antagonist known to disrupt reconsolidation (Dębiec and LeDoux 2004;Kindt et al 2009;Soeter and Kindt 2010), 90 min prior to selective reactivation of the CS1 memory (day 2).…”

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confidence: 99%

Disrupting reconsolidation: Pharmacological and behavioral manipulations

Soeter

Kindt²

2011

Learn. Mem.

246

332

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We previously demonstrated that disrupting reconsolidation by pharmacological manipulations "deleted" the emotional expression of a fear memory in humans. If we are to target reconsolidation in patients with anxiety disorders, the disruption of reconsolidation should produce content-limited modifications. At the same time, the fear-erasing effects should not be restricted to the feared cue itself considering that fear generalization is a main characteristic of anxiety disorders. In Experiment I and Experiment I b , we addressed these issues using a within-subject differential startle fear conditioning paradigm and a test of fear generalization. In Experiment II, we tested whether a behavioral approach targeting the reconsolidation through extinction learning was also effective in weakening the original fear memory. A behavioral procedure is evidently preferred over drug manipulations provided that similar effects can be obtained. Here, the extinction procedure subsequent to retrieval did not "erase" the emotional expression of the fear memory as the retrieval techniques (i.e., reminder shocks and reacquisition) unveiled a return of the startle fear response to the fear-relevant stimuli. In contrast, b-adrenergic receptor blockade during reconsolidation selectively deleted the fear-arousing aspects of the memory (i.e., startle fear response) along with its category-related information. The pharmacological manipulation rendered the core memory trace too weak to observe fear generalization after successful reacquisition. Hence, relearning following the disruption of reconsolidation seems to be qualitatively different from initial learning. Our findings demonstrate that disrupting reconsolidation by pharmacological manipulations, although selective, undermines the generalization of fear, a key feature of anxiety disorders.[Supplemental material is available for this article.]The phenomenon of reconsolidation, the stabilization of a memory after retrieval, enables the modification of memory representation (Nader et al. 2000). Considerable evidence in animals now indicates that blockade of the process of reconsolidation by pharmacological manipulations produces amnesia for the original fear learning (Nader et al. 2000;Dudai 2006;Tronson and Taylor 2007;Nader and Hardt 2009). We previously demonstrated that disrupting reconsolidation by administering propranolol prior to memory reactivation resulted in erasure of the fear response in humans (Kindt et al. 2009), an effect that persisted over time (Soeter and Kindt 2010). However, the typical differential fear conditioning paradigm (i.e., CS1-US vs. CS2) did not allow any inference about the nature of the fear memory erasure. Even though animal studies showed selective amnesia for the specific fear association (i.e., CS1-US) (Doyère et al. 2007), studying humans necessitates systemic (as opposed to intra-amygdala) drug administration. Accordingly, the erasure of the fear response could also have resulted from a more diffuse effect of the propranolol manipulation by reduc...

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Electrodermal and subjective reactions to fear-relevant stimuli under threat of shock

Cited by 15 publications

References 32 publications

Cognitive Processes in Extinction: Figure 1

Cognitive Processes in Extinction: Figure 1

Stimulation of the Noradrenergic System during Memory Formation Impairs Extinction Learning but not the Disruption of Reconsolidation

Disrupting reconsolidation: Pharmacological and behavioral manipulations

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