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

Philip R Corlett¹, Garry D Honey, John H Krystal

¹Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06519, USA. philip.corlett@yale.edu

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology

|September 24, 2010

Summary

This summary is machine-generated.

Ketamine alters conscious experience by disrupting brain learning and inference processes, mimicking psychosis symptoms. Individual differences in these processes explain varied ketamine effects, offering insights into psychosis.

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Area of Science:

Neuroscience
Psychiatry
Cognitive Science

Background:

Glutamatergic neurotransmission modulation affects conscious experience, inducing psychosis-like symptoms.
Ketamine, an NMDA receptor antagonist, is used to study these alterations.
Interindividual variability in ketamine's effects is significant and requires explanation.

Purpose of the Study:

To review studies on intravenous ketamine administration and its effects on conscious experience.
To explore individual variability in ketamine's profound effects within a learning and inference model.
To understand the neurobiological underpinnings of psychosis symptoms through ketamine's action.

Main Methods:

Review of existing scientific literature on ketamine administration and its psychological effects.
Application of a hypothetical Bayesian brain model focusing on learning and inference.
Analysis of N-methyl-D-aspartate (NMDA) receptor blockade and glutamatergic signaling.

Main Results:

Ketamine temporarily disrupts the brain's ability to specify expectations and signal expectancy violations.
NMDA blockade and altered glutamatergic signaling are key mechanisms.
Individual differences in neural circuits for learning and inference contribute to varied ketamine experiences.

Conclusions:

Individual variability in ketamine's effects may stem from genetic and experiential factors influencing learning and inference.
Chronic NMDA blockade has more profound and lasting effects on expectancy specification than acute blockade.
Studying these individual differences within a Bayesian framework can illuminate psychosis mechanisms.