Evidence map›Paper›PMID 20861831›Full record

ReviewNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2011

Glutamatergic model psychoses: prediction error, learning, and inference.

Philip R Corlett, Garry D Honey, John H Krystal, Paul C Fletcher

Abstract readReview
In one paragraph

Review in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

101 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  7. Mismatch negativity encoding of prediction errors predicts S-ketamine-induced cognitive impairments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
    Trial
  8. Psychedelic-Related Psychosis: From Model Psychosis to Psychotherapy.Current topics in behavioral neurosciences · 2026
    Review
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  12. Article
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  15. Review
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  18. Synthetic surprise as the foundation of the psychedelic experience.Neuroscience and biobehavioral reviews · 2024
    Review
  19. Article
  20. Resolving the Delusion Paradox.Schizophrenia bulletin · 2023
    Review

41 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Philip R CorlettDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT 06519, USA. philip.corlett@yale.edu
Garry D Honey
John H Krystal
Paul C Fletcher

Funding

Wellcome Trust 064351
6 · The paper itself

Abstract

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.

Indexed as

Models, NeurologicalAnimalsBayes TheoremCognitionExcitatory Amino Acid AntagonistsGlutamic AcidHumansLearningPsychoses, Substance-InducedPsychotic DisordersReceptors, GlutamateExcitatory Amino Acid AntagonistsGlutamic AcidReceptors, Glutamate

Identifiers

PMID20861831
PMCPMC3055519

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.