An Effective Paradigm for Conditioning Visual Perception in Human Subjects

Davies, Peter; Davies, G. L.; Bennett, Spencer

doi:10.1068/p110663

Cited by 17 publications

(18 citation statements)

References 6 publications

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“…Pavlov equated the learned conditioned reflexes that he observed with Helmholtz' learned perceptual expectancies (Barlow, 1990;Helmholtz, 1878Helmholtz, /1971, an assertion supported by empirical evidence (Davies et al, 1982). Such conditioned expectancies are also important for causal inference and belief formation (Dickinson, 2001); in particular, we learn most in situations that violate our expectancies, inducing prediction error (Rescorla and Wagner, 1972); we attend most to features that are coincident with prediction error (Pearce and Hall, 1980) and we use prediction errors to learn the parameters of causal models as well as which causal models are able to explain the co-occurrence of particular events (Waldmann and Martignon, 1998).…”

Section: Pðhjdþ ¼ Pðdjhþpðhþ Pðdþmentioning

confidence: 53%

Glutamatergic Model Psychoses: Prediction Error, Learning, and Inference

Corlett

Honey

Krystal

et al. 2010

Neuropsychopharmacol

214

173

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Modulating glutamatergic neurotransmission induces alterations in conscious experience that mimic the symptoms of early psychotic illness. We review studies that use intravenous administration of ketamine, focusing on interindividual variability in the profundity of the ketamine experience. We will consider this individual variability within a hypothetical model of brain and cognitive function centered upon learning and inference. Within this model, the brains, neural systems, and even single neurons specify expectations about their inputs and responding to violations of those expectations with new learning that renders future inputs more predictable. We argue that ketamine temporarily deranges this ability by perturbing both the ways in which prior expectations are specified and the ways in which expectancy violations are signaled. We suggest that the former effect is predominantly mediated by NMDA blockade and the latter by augmented and inappropriate feedforward glutamatergic signaling. We suggest that the observed interindividual variability emerges from individual differences in neural circuits that normally underpin the learning and inference processes described. The exact source for that variability is uncertain, although it is likely to arise not only from genetic variation but also from subjects' previous experiences and prior learning. Furthermore, we argue that chronic, unlike acute, NMDA blockade alters the specification of expectancies more profoundly and permanently. Scrutinizing individual differences in the effects of acute and chronic ketamine administration in the context of the Bayesian brain model may generate new insights about the symptoms of psychosis; their underlying cognitive processes and neurocircuitry.

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Section: Pðhjdþ ¼ Pðdjhþpðhþ Pðdþmentioning

confidence: 53%

Glutamatergic Model Psychoses: Prediction Error, Learning, and Inference

Corlett

Honey

Krystal

et al. 2010

Neuropsychopharmacol

214

173

View full text Add to dashboard Cite

show abstract

“…Y Conditioned afterimages. It has been reported that visual experiences (in the absence of visual input) can be elicited as conditioned responses to tones after pairing images with tones (49). This finding would demonstrate a conditioned visual response but not one that occurs during normal vision.…”

Section: Discussionmentioning

confidence: 74%

Demonstration of cue recruitment: Change in visual appearance by means of Pavlovian conditioning

Saunders

Stone

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

100

161

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“…Pavlov believed that one could equate his conditioned reflexes with Helmholtz' learned perceptual expectancies (Barlow, 1990; Helmholtz, 1871/1971), an assertion supported by empirical evidence (Davies et al, 1982). Recently, computational neuroscientists have also come to appreciate the overlap between learning and perception, emphasizing the consilience between formal theories of conditioning, Bayesian accounts of learning and signal detection theories of perceptual decision making (Dayan and Daw, 2008).…”

Section: Internal Reinforcement Hypothesis and Delusionsmentioning

confidence: 97%

Why do delusions persist?

Corlett

2009

Front. Hum. Neurosci.

127

109

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Delusions are bizarre and distressing beliefs that characterize certain mental illnesses. They arise without clear reasons and are remarkably persistent. Recent models of delusions, drawing on a neuroscientific understanding of learning, focus on how delusions might emerge from abnormal experience. We believe that these models can be extended to help us understand why delusions persist. We consider prediction error, the mismatch between expectancy and experience, to be central. Surprising events demand a change in our expectancies. This involves making what we have learned labile, updating and binding the memory anew: a process of memory reconsolidation. We argue that, under the influence of excessive prediction error, delusional beliefs are repeatedly reconsolidated, strengthening them so that they persist, apparently impervious to contradiction.

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An Effective Paradigm for Conditioning Visual Perception in Human Subjects

Cited by 17 publications

References 6 publications

Glutamatergic Model Psychoses: Prediction Error, Learning, and Inference

Glutamatergic Model Psychoses: Prediction Error, Learning, and Inference

Demonstration of cue recruitment: Change in visual appearance by means of Pavlovian conditioning

Why do delusions persist?

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