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Table of Contents
Vol. 66, No. 1, 2012
Issue release date: July 2012
Section title: Paper
Neuropsychobiology 2012;66:33–43
(DOI:10.1159/000337132)

Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

Pankow A. · Knobel A. · Voss M. · Heinz A.
aDepartment of Psychiatry and Psychotherapy, Campus Charité Mitte, bCluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, and cBernstein Center of Computational Neuroscience, Berlin, Germany

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Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 6/1/2011 7:22:47 PM
Accepted: 1/30/2012
Published online: 7/13/2012

Number of Print Pages: 11
Number of Figures: 1
Number of Tables: 3

ISSN: 0302-282X (Print)
eISSN: 1423-0224 (Online)

For additional information: http://www.karger.com/NPS

Abstract

Dopamine dysfunction is a mainstay of theories aimed to explain the neurobiological correlates of schizophrenia symptoms, particularly positive symptoms such as delusions and passivity phenomena. Based on studies revealing dopamine dysfunction in addiction research, it has been suggested that phasic or chaotic firing of dopaminergic neurons projecting to the (ventral) striatum attribute salience to otherwise irrelevant stimuli and thus contribute to delusional mood and delusion formation. Indeed, several neuroimaging studies revealed that neuronal encoding of usually irrelevant versus relevant stimuli is blunted in unmedicated schizophrenia patients, suggesting that some stimuli that are irrelevant for healthy controls acquire increased salience for psychotic patients. However, salience attribution per se may not suffice to explain anxieties and feelings of threat that often accompany paranoid ideation. Here, we suggest that beyond ventral striatal dysfunction, dopaminergic dysregulation in limbic areas such as the amygdala in interaction with prefrontal and temporal cortex may contribute to the formation of delusions and negative symptoms. Neuroleptic medication, on the other hand, appears to interfere with anticipation of reward in the ventral striatum and can thus contribute to secondary negative symptoms such as apathy and avolition.


Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 6/1/2011 7:22:47 PM
Accepted: 1/30/2012
Published online: 7/13/2012

Number of Print Pages: 11
Number of Figures: 1
Number of Tables: 3

ISSN: 0302-282X (Print)
eISSN: 1423-0224 (Online)

For additional information: http://www.karger.com/NPS


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