Pavlovian conditioning and its proper control procedures.

Rescorla, Robert A.

doi:10.1037/h0024109

Cited by 1,329 publications

(777 citation statements)

References 12 publications

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“…This most obviously applies to the frequently used (and most effective) protocol in which a CS that previously was paired with the US on 100% of its occurrences subsequently is presented repeatedly without further US delivery. However, other protocols that produce a decrement in conditioned responding include ones in which the US continues to be presented but occurs in an explicitly unpaired or random arrangement with the CS; [10][11][12] ones in which the CS is reinforced on a smaller percentage of its presentations than it was during acquisition (as with a shift from 100 to 50% reinforcement; 13 or even ones in which the US continues to be paired with the CS on 100% of its presentations but the intensity of the US is diminished relative to what it was during acquisition 14,15 or to what it was 'expected' to be on the basis of acquisition. 16 Hence, a critical determining factor for extinction to occur seems to be a violation of the 'expected' contingency between the CS and the US experienced in earlier stages of training.…”

Section: Behavioral and Theoretical Considerationsmentioning

confidence: 99%

Mechanisms of fear extinction

2006

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Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications. Molecular Psychiatry (2007) 12, 120-150.

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Section: Behavioral and Theoretical Considerationsmentioning

confidence: 99%

Mechanisms of fear extinction

2006

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“…In the first pretraining session, 60 presentations of each tone without the foot shock US were given, with the same timing and ordering as during training. The same schedule of tone presentations with the addition of explicitly unpaired US presentations (see Rescorla, 1967) were given in the second pretraining session. In this session the US was not presented during a tone or within three seconds before or after a tone presentation.…”

Section: Methodsmentioning

confidence: 99%

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

Poremba

Gabriel

1997

J. Neurosci.

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This study assessed the role of the thalamic medial geniculate (MG) nucleus in discriminative avoidance learning, wherein rabbits acquire a locomotory response to a tone [conditioned stimulus (CS)ϩ] to avoid a foot shock, and they learn to ignore a different tone (CSϪ) not predictive of foot shock. Limbic (anterior and medial dorsal) thalamic, cingulate cortical, or amygdalar lesions severely impair acquisition, and neurons in these areas develop training-induced activity (TIA): more firing to the CSϩ than to the CSϪ. MG neurons exhibit TIA during learning and project to the amygdala. The MG neurons may supply afferents essential for amygdalar and cingulothalamic TIA and for avoidance learning. To test this hypothesis, bilateral electrolytic or excitotoxic ibotenic acid MG nuclear lesions were induced, and multiunit recording electrodes were chronically implanted into the anterior and posterior cingulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei, and the basolateral nucleus of the amygdala before training. Learning was severely impaired and TIA was abolished in all areas in rabbits with lesions. Thus learning and TIA require the integrity of the MG nucleus. Only damage in the medial MG division was significantly correlated with the learning deficit. The lesions abolished the sensory response of amygdalar neurons, and they attenuated (but did not eliminate) the sensory response of cingulothalamic neurons, suggesting the existence of extra geniculate sources of auditory transmission to the cingulothalamic areas. Key words: limbic thalamus; cingulate cortex; amygdala; learning; instrumental conditioning; anterior ventral nucleus; medial dorsal nucleusThere is currently a great interest in the neural circuitry underlying aversively motivated learning (for review, see Davis, 1992;Gabriel, 1993;Lennartz and Weinberger, 1994;LeDoux, 1995;McGaugh et al., 1995;. A central role of amygdalar neurons is indicated by findings that amygdala lesions impair the acquisition of conditioned immobility (LeDoux et al., 1988; Fanselow and K im, 1994;LeDoux, 1995), autonomic responding (Blanchard and Blanchard, 1972;Spevack et al., 1975;Kapp et al., 1979;Gentile et al., 1986;Iwata et al., 1986;Helmstetter, 1992) and fear-potentiated startle behavior (Davis, 1986(Davis, , 1992Hitchcock and Davis, 1987;Sananes and Davis, 1992). Also, amygdalar neurons exhibit associative, training-induced activity (TIA) during Pavlovian conditioning (Umemoto and Olds, 1975;Applegate et al., 1982;Pascoe and Kapp, 1985;Nishijo et al., 1988; Muramoto et al., 1993;McEchron et al., 1995;Quirk et al., 1995).An involvement of the medial geniculate (MG) nucleus in aversively motivated learning is indicated by the observation of TIA in the medial division of the MG nucleus (MGm) (Olds et al., 1972;Gabriel et al., 1975;Gabriel et al., 1976;Ryugo and Weinberger, 1978;Birt and Olds, 1981;Weinberger, 1982;Edeline, 1990;Edeline and Weinberger, 1992;McEchron et al., 1995), and by impaired conditioning in animals with MG lesions (Iwata et al., 198...

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“…inhibition of delay; Pavlov, 1927). On the other hand, when the CS and US presentations are uncorrelated (truly random control), no conditioning occurs (Rescorla, 1967). Moreover, because the US occurs at random times in the CS, timing of the US should not occur.…”

Section: Introductionmentioning

confidence: 99%

Are separate theories of conditioning and timing necessary?

Kirkpatrick

Church

1998

Behavioural Processes

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Conditioning and timing studies have evolved under separate traditions, which is exemplified in both traditional theories (e.g. the Rescorla-Wagner model of conditioning vs. Scalar Timing Theory) and in a dual process model (Gibbon, J., Balsam, P., 1981. In: Autoshaping and Conditioning Theory. Academic Press, New York.). Other lines of theoretical development in both timing and conditioning fields have resulted in the emergence of 'hybrid' theories in which conditioning and timing processes are integrated. Simulations were conducted with a recent hybrid theory of timing (Machado, A., 1997. Psychol. Rev. 104, 241 -265). The simulations were of classical conditioning procedures in which the local or global predictability of food was varied by manipulating the variability of the CS-US relationship, variability of the CS duration, and variability of the intertrial interval. The hybrid model provided good qualitative fits to indices of conditioning (discrimination ratios) and timing (local rates of responding), indicating that it may be possible to model both conditioning and timing results with a single process in which an internal representation of time and a strength of association are integrated. However, the failure of the model to provide good quantitative fits of the data indicates the need for a consideration of alternative perceptual representations of time and/or principles of association within the framework of the hybrid model.

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Pavlovian conditioning and its proper control procedures.

Cited by 1,329 publications

References 12 publications

Mechanisms of fear extinction

Mechanisms of fear extinction

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

Are separate theories of conditioning and timing necessary?

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