Eysenck's theory of incubation: An empirical test

Nicholaichuk, Terrence P.; Quesnel, Lionel J.; Tait, Robert W.

doi:10.1016/0005-7967(82)90092-4

Cited by 21 publications

(6 citation statements)

References 19 publications

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“…However, mice treated with propanolol, an antagonist of adrenergic ␤ receptors, uncovers persistent increases of fear at test, while yohimbine, an antagonist of presynaptic, autoinhibitory ␣ 2 receptors, yields significant extinction after spaced CS presentations (Cain et al 2004). Others have made similar observations of "incubation" following CS presentations, although there have also been failures of replication (Eysenck 1968;Rohrbaugh and Riccio 1970;Silvestri et al 1970;Morley 1977;Nicholaichuk et al 1982;Markus and Canavan 1985;Sandin and Chorot 1989). The data in this study (Fig.…”

Section: Discussionsupporting

confidence: 61%

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Ponnusamy¹,

Nissim²,

Barad³

2005

Learn. Mem.

123

101

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Extinction of conditioned fear in animals is the explicit model of behavior therapy for human anxiety disorders, including panic disorder, obsessive-compulsive disorder, and post-traumatic stress disorder. Based on previous data indicating that fear extinction in rats is blocked by quinpirole, an agonist of dopamine D2 receptors, we hypothesized that blockade of D2 receptors might facilitate extinction in mice, while agonists should block extinction, as they do in rats. One day after fear conditioning mice with three pairings of a white noise conditional stimulus (CS) with moderate footshock, we injected the D2 antagonist, sulpiride, the D2 agonist, quinpirole, or vehicle, just before repeated CS presentations to generate extinction. We assayed fear by measuring behavioral freezing during extinction presentations and then drug-free during CS presentations 1 d later. We found that sulpiride injections before extinction training facilitated extinction memory 24 h later, while quinpirole partially blocked extinction memory compared with vehicle-injected controls. Notably, sulpiride treatment yielded significant extinction after spaced CS presentations, which yield no extinction at all in vehicle-treated mice. These findings suggest that dopamine D2-mediated signaling contributes physiological inhibition of extinction, and that D2 antagonists may be useful adjuncts to behavior therapy of human anxiety disorders.Extinction of conditioned fear in mammals is an important preclinical model of behavior therapy, one of the most effective treatments for human anxiety disorders (Wolpe 1969;Craske 1999). Despite the efficacy of behavior therapy for human anxiety disorders, extinction-like treatments require repeated cue exposures and are vulnerable to reversal by a number of environmental factors. Thus, a deeper understanding of the synaptic mechanisms of extinction may permit the development of adjunctive medications to facilitate extinction learning, and perhaps, to make it more permanent.Anxiety disorders affect about 16% of the American population and include panic disorder (PD, 1.7%), obsessivecompulsive disorder (OCD, 2.3%), post-traumatic stress disorder (PTSD, 3.6%), generalized anxiety disorder (GAD, 2.8%), social phobia (2%), and simple phobias (8%) (US-Surgeon-General 1999). The rate of PTSD may well go higher in the context of current wars and terrorist acts. Given the enormous burden of such anxiety disorders, we are fortunate in having a reasonable animal model for the acquisition of some of these fears, that is, classically conditioned fear, and an even better animal model of an effective treatment method for those disorders, extinction of conditioned fear.Pavlovian, or classical, fear conditioning has long been an important model both of associative learning and of the etiology of human anxiety (Watson and Rayner 1920;Eysenck 1979;Wolpe and Rowan 1988). Temporal pairing of a neutral conditional stimulus (CS) with an aversive unconditional stimulus (US) generates robust conditional fear responses upon subseque...

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Section: Discussionsupporting

confidence: 61%

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Ponnusamy¹,

Nissim²,

Barad³

2005

Learn. Mem.

123

101

View full text Add to dashboard Cite

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“…Since Eysenck (1968) termed this phenomenon “incubation,” some studies have provided tentative support for this hypothesis (e.g., Rohrbaugh and Riccio, 1970; Rohrbaugh et al, 1972). Until now, little evidence exists that repeated CS-only presentations promote a progressive increase in CR strength (Nicholaichuk et al, 1982; Kaloupek, 1983). Most studies demonstrate that short duration CS-presentations evoke resistance to extinction, rather than incubation (Stone and Borkovec, 1975; Sandin and Chorot, 1989).…”

Section: Methodsmentioning

confidence: 99%

Repeated Activation of a CS-US-Contingency Memory Results in Sustained Conditioned Responding

Joos¹,

Vansteenwegen²,

Vervliet³

et al. 2013

Front. Psychol.

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Individuals seem to differ in conditionability, i.e., the ease by which the contingent presentation of two stimuli will lead to a conditioned response. In contemporary learning theory, individual differences in the etiology and maintenance of anxiety disorders are, among others, explained by individual differences in temperamental variables (Mineka and Zinbarg, 2006). One such individual difference variable is how people process a learning experience when the conditioning stimuli are no longer present. Repeatedly thinking about the conditioning experience, as in worry or rumination, might prolong the initial (fear) reactions and as such, might leave certain individuals more vulnerable to developing an anxiety disorder. However, in human conditioning research, relatively little attention has been devoted to the processing of a memory trace after its initial acquisition, despite its potential influences on subsequent performance. Post-acquisition processing can be induced by mental reiteration of a conditioned stimulus-unconditioned stimulus (CS-US)-contingency. Using a human conditioned suppression paradigm, we investigated the effect of repeated activations of a CS-US-contingency memory on the level of conditioned responding at a later test. Results of three experiments showed more sustained responding to a “rehearsed” CS+ as compared to a “non-rehearsed” CS+. Moreover, the second experiment showed no effect of rehearsal when only the CS was rehearsed instead of the CS-US-contingency. The third experiment demonstrated that mental CS-US-rehearsal has the same effect regardless of whether it was cued by the CS and a verbal reference to the US or by a neutral signal, making the rehearsal “purely mental.” In sum, it was demonstrated that post-acquisition activation of a CS-US-contingency memory can impact conditioned responding, underlining the importance of post-acquisition processes in conditioning. This might indicate that individuals who are more prone to mentally rehearse information condition more easily.

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“…Some, like the partial irreversibility of fear account (Solomon & Wynne, 1954), involve subde tailoring of Mowrer's theory and seem simply post hoc descriptions of the data rather than explanations of it (Rachman, 1976). Others, like the incubation account (Eysenck, 1979), have proved popular but lack any real experimental support (see further, Bersh, 1980;Kimmel, 1979;McAllister & McAllister, 1979;Nicholaichuk, Quesnel, & Tait, 1982). Some, like the serial CS hypothesis (Stampfl, 1991) lack support in clinical samples, whereas others, like the safety-signal account (Rachman, 1983(Rachman, , 1984, seem applicable to only certain phobic disorders (Mattick, 1987;Rachman, 1984).…”

Section: The Classical Conditioning Accountmentioning

confidence: 99%

The etiology of phobias: a nonassociative account

Menzies

Clarke

1995

Clinical Psychology Review

196

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ABSTRACT. Theories of the origin and maintenance of fears and phobias have had a profound influence on the kinds of treatments employed in the phobicINCREASINGLY, clinicians and researchers alike are recognising the need to collect information about the origins of phobic cases as a standard part of initial assessment. This information enables the researcher to evaluate the relevance of the various theoretical approaches, and may provide useful data for the clinician who must choose an appropriate treatment strategy. It has been argued that different modes of onset may lead to different individual response patterns and result in differential response to standard treatments (Rachman, 1977). Thus, theories of the origin and maintenance of fears and phobias continue to have a profound influence on the kinds of treatments employed with phobic patients. It is largely in view of this influence that the present paper focuses on the major etiological accounts, beginning with a review of the traditional conditioning model and the psychoanalytic account that it sought to replace.

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Eysenck's theory of incubation: An empirical test

Cited by 21 publications

References 19 publications

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Repeated Activation of a CS-US-Contingency Memory Results in Sustained Conditioned Responding

The etiology of phobias: a nonassociative account

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