The partial reinforcement extinction effect in humans: effects of schizophrenia, schizotypy and low doses of amphetamine

Abstract

The partial reinforcement extinction effect (PREE) was studied in human subjects. It has been suggested that the PREE depends on neural mechanisms critical to the cognitive dysfunction which underlines acute schizophrenia. We therefore predicted that the PREE should be reduced, through decreased resistance to extinction in the partial reinforcement (PR) condition, in various types of individual: (a) healthy volunteers given low doses of oral amphetamine; (b) those in the acute (but not chronic) phase of a schizophrenic illness and; (c) healthy volunteers with high scores on personality measures of schizotypy. Despite obtaining robust demonstrations of PREE in all experiments, none of these predictions were confirmed. A single, low dose, of amphetamine had no effect on either continuous reinforcement (CR) or partial reinforcement (PR). Acute and chronic schizophrenic patients showed a reduced PREE compared to controls. However this was due to increased resistance to extinction in the CR groups. Finally, high schizotypy scores were associated with greater PREE, attributable to both decreased extinction in the CR condition and increased extinction in the PR condition. The results of these experiments on human PREE provide no support that PREE is a valid paradigm with which to explore the cognitive dysfunction underlying schizophrenia.