Spontaneous recovery of extinguished fear responses deepens their extinction: A role for error-correction mechanisms.

Leung, Hiu Tin; Westbrook, R. Frederick

doi:10.1037/0097-7403.34.4.461

Cited by 51 publications

(63 citation statements)

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“…One such manipulation is the passage of time between nonreinforced exposures, which has been suggested to promote further inhibitory learning by restoring prediction error when an already exposed stimulus is given additional exposures (Leung and Westbrook, 2008). Consistent with this suggestion, in latent inhibition, rats given an initial bout of preexposure to a stimulus and then given additional exposures after a passage of time showed more latent inhibition than a stimulus given equivalent but successive exposures (Holtzman et al, 2010).…”

Section: Introductionsupporting

confidence: 58%

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

Leung

Killcross

Westbrook

2013

Neuropsychopharmacol

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Latent inhibition refers to the retardation in the development of conditioned responding when a pre-exposed stimulus is used to signal an unconditioned stimulus. This effect is described by error-correction models as an attentional deficit and is commonly used as an animal model of schizophrenia. A series of experiments studied the role of error-correction mechanism in latent inhibition and its interaction with the endogenous opioid system. Systemic administration of the competitive opioid receptor antagonist naloxone before rats were pre-exposed to a target stimulus prevented latent inhibition of its subsequent fear conditioning; it was without effect on a non-preexposed stimulus and did not produce state-dependent learning (Experiments 1a and 1b). Naloxone did not reverse the latent inhibitory effect already accrued to a pre-exposed target. However, it did prevent the enhancement of latent inhibition by a long retention interval interpolated between its initial exposure and re-exposure (Experiment 2) or by a novel stimulus compounded with the pre-exposed target during re-exposure (Experiment 3). These results provide evidence that attentional loss in latent inhibition is instructed by an opioid-mediated error signal which diminishes with repeated stimulus exposures but recovers with the passage of time or reintroduction of novelty.

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Section: Introductionsupporting

confidence: 58%

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

Leung

Killcross

Westbrook

2013

Neuropsychopharmacol

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“…Rescorla (2003) also found that response loss to a cue extinguished in compound with a familiar but neutral stimulus was greater than that to a cue extinguished in compound with a conditioned inhibitor. Finally, Leung and Westbrook (2008) reported greater loss of responding to a cue that was extinguished in compound with an extinguished cue undergoing spontaneous recovery (error was large) than to a second cue extinguished in compound with an extinguished cue not undergoing recovery (error was small).…”

Section: Introductionmentioning

confidence: 99%

A common error term regulates acquisition but not extinction of causal judgments in people

Griffiths

Westbrook

2011

Learn Behav

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In three experiments, we used the allergist task to examine the role of error correction mechanisms in the acquisition and extinction of causal judgments in people. Consistent with existing human and animal studies, acquisition of causal judgments was influenced by the discrepancy between the allergenic outcome and that predicted by all of the cues present on a trial (the "common error" term). However, in the present experiments, we failed to detect any evidence for the use of a common error term in extinction learning: Judgments of the allergenic properties of a cue were unaffected by the predictive value of the other cues present on a trial. This asymmetry in the use of a common error term in acquisition and extinction learning is inconsistent with previous animal studies and also with most models of associative learning. However, approaches that allow learning to be specific to a particular arrangement of elemental cues (context specific and state based) offer some explanation of the observed asymmetry.Keywords Human causal learning . Extinction . Associative learning Contemporary theories of associative learning invoke error correction mechanisms to explain a range of Pavlovian acquisition phenomena in animal subjects. These theories originate in the blocking, contingency, and signal validity effects reported in the classic experiments by Kamin (1969), Rescorla (1969), andWagner (1969), respectively. Each of these experiments demonstrated that learning about a conditioned stimulus (CS X) depends not only on its relation to a motivationally significant outcome [an unconditioned stimulus (US)] but also on the relation between other concomitantly present cues (CSA) and the US. More specifically, each demonstrated that a relation between X and the US, which was normally effective in producing learning, was rendered ineffective by the presence of a better predictor (A) of the US. Learning about X was reduced when pairings of an AX compound and the US were preceded by pairings of A and the US (Kamin, 1969), when X-US pairings were interspersed with US-alone presentations in the context (A) where the pairings occurred (Rescorla, 1969), and when X was paired with the US in the presence of A but not B relative to when X was equally often paired or not paired with the US in the presence of A and B (Wagner, 1969). These effects led to the development of theories (e.g., Pearce & Hall, 1980;Rescorla & Wagner, 1972;Wagner, 1981) whose central proposals are that associative formation is regulated by the discrepancy between the actual and predicted outcome of a trial and that all of the cues present are used to calculate the discrepancy whose size determines associative change. These theories have not only explained the blocking, contingency, and signal validity effects as well as other existing Pavlovian acquisition phenomena (e.g., overshadowing and conditioned inhibition), but have also successfully predicted new ones (e.g., over expectation and super conditioning). Dickinson, Shanks, and Evenden (1984) noted the...

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“…Just as extinction leaves intact the excitatory association produced by conditioning, recent evidence also shows that reconditioning an extinguished CS leaves intact the inhibitory association produced by extinction. For instance, such a CS continues to exhibit the signature phenomena of extinction such as spontaneous recovery (Rescorla 2001;Leung and Westbrook 2008). This implies that the learning that produces these phenomena survives reconditioning in spite of the fact that the CS now elicits fear responses (see Rescorla [2001], for discussion).…”

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confidence: 99%

Systemic or intra-amygdala injection of a benzodiazepine (midazolam) impairs extinction but spares re-extinction of conditioned fear responses

Hart¹,

Harris²,

Westbrook³

2009

Learn. Mem.

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Rats were subjected to one or two cycles of fear conditioning and extinction, injected with a benzodiazepine, midazolam, before the first or second extinction, and tested for long-term inhibition of fear responses (freezing). In Experiment 1, inhibition of context-conditioned fear was spared when midazolam was injected before the second extinction, but impaired when injected before the first. In Experiment 2, it was spared when midazolam was injected before the second extinction, but only if vehicle had been injected before the first: Inhibition was impaired when the drug was injected before both. In Experiment 3, inhibition of a discrete conditioned stimulus (CS A) was spared when midazolam was injected before its second extinction, but impaired when injected before extinction of CS A in rats that had undergone extinction of CS B. In Experiment 4, inhibition was spared when midazolam was injected into the basolateral amygdala before the second extinction, but impaired when injected before the first extinction of context-conditioned fear. The results show that midazolam impairs learning, but not relearning to inhibit fear responses, and are discussed in terms of state dependency, error correction, and memory retrieval, whereby the drug's anxiolytic effects on the second extinction reactivate and strengthen the original inhibitory memory.Clinical trials have established the effectiveness of cognitivebehavioral therapy for anxiety disorders such as posttraumatic stress (Harvey et al. 2003). A component of this therapy is cue exposure in which the patient, aided by the clinician, confronts trauma-related cues in the absence of overt danger. One aim of these confrontations is to reduce, even eliminate, the ability of the trauma-related cues to elicit the fear memories that are undermining the quality of the patient's life. This aim is frequently achieved. However, the psychological processes and neural mechanisms that underlie the successes of cue exposure or that are responsible for its failures are poorly understood. Therefore, there has been much interest in laboratory models of cue exposure. One model is the extinction of Pavlovian conditioned fear responses.

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Spontaneous recovery of extinguished fear responses deepens their extinction: A role for error-correction mechanisms.

Cited by 51 publications

References 34 publications

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

A common error term regulates acquisition but not extinction of causal judgments in people

Systemic or intra-amygdala injection of a benzodiazepine (midazolam) impairs extinction but spares re-extinction of conditioned fear responses

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