Dopaminergic dysfunction in alcoholism and schizophrenia – psychopathological and behavioral correlates

  title={Dopaminergic dysfunction in alcoholism and schizophrenia – psychopathological and behavioral correlates},
  author={Andreas Heinz},
  journal={European Psychiatry},
  pages={9 - 16}
  • A. Heinz
  • Published 1 March 2002
  • Psychology, Medicine, Biology
  • European Psychiatry

Dopaminergic dysfunction in schizophrenia: salience attribution revisited.

It is suggested that neuronal functions associated with dopaminergic signaling, such as the attribution of salience to reward-predicting stimuli and the computation of prediction errors, are indeed altered in schizophrenia patients and that this impairment appears to contribute to delusion formation.

From apathy to addiction: Insights from neurology and psychiatry

Treatment effects in schizophrenia : evidence from neuroimaging

  • Psychology, Biology
  • 2012
The hypothesis that improvements in the symptomatology are related to neurobiological modifications is supported, especially in frontal, striatal and parietal areas as well as the amygdala.

Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

It is suggested 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.

Striatal involvement in human alcoholism and alcohol consumption, and withdrawal in animal models.

Alterations of dopaminergic, glutamatergic, and GABAergic signaling within different regions of the striatum by alcohol is critical for alcohol craving, consumption, dependence, and withdrawal in humans and animal models.

Presynaptic Dopaminergic Function: Implications for Understanding Treatment Response in Psychosis

All current antipsychotic drugs block dopamine (DA) receptors, but the nature of the DA dysfunction in schizophrenia has not been clear. However, consistent evidence now shows that presynaptic

Striatal Dopamine and Reward Prediction Error Signaling in Unmedicated Schizophrenia Patients

A dissociation between striatal subregions and symptom domains is suggested, with elevated dopamine synthesis capacity in the associative striatum contributing to positive symptoms while blunted prediction error signaling in the ventral striatum related to negative symptoms.

Improvement of brain reward abnormalities by antipsychotic monotherapy in schizophrenia.

The first controlled, longitudinal study of reward disturbances in schizophrenic patients before and after their first antipsychotic treatment demonstrates that alterations in reward processing are fundamental to the illness and are seen prior to any treatment.

Reward system activation in schizophrenic patients switched from typical neuroleptics to olanzapine

Failure to activate the ventral striatum during reward anticipation was pharmacologically state-dependent and observed only in patients treated with typical neuroleptics but not with olanzapine, which may indicate that this drug did not induce secondary negative symptoms via interference with reward anticipation.



Psychopathological correlates of reduced dopamine receptor sensitivity in depression, schizophrenia, and opiate and alcohol dependence.

The findings indicate that patients with dopaminergic dysfunction are not unable to experience pleasure, but may fail to be motivated by environmental stimuli to seek reward.

Serotonergic dysfunction, negative mood states, and response to alcohol.

Several lines of evidence point to a relationship between serotonergic dysfunction, negative mood states, and excessive alcohol intake, which may be mediated in part by reduced alcohol-induced sedation.

Psychopathological and behavioral correlates of dopaminergic sensitivity in alcohol-dependent patients.

This study did not support the hypothesis that reduced sensitivity of dopamine receptors is associated with anxiety, depressed mood, or high novelty seeking in alcoholism.

Dopamine transporters increase in human brain after alcohol withdrawal

The data indicate that prolonged heavy drinking decreases da transporter binding and distrubs synaptic dopamine transport, which may sensitize alcoholics to dopaminergic transmission, which could lead to early relapse after ethanol withdrawal.

Positron emission tomography reveals elevated D2 dopamine receptors in drug-naive schizophrenics.

Schizophrenia itself is associated with an increase in brain D2 dopamine receptor density, and the densities in the caudate nucleus were higher in both groups of patients than in the normal volunteers.

The glutamatergic basis of human alcoholism.

A host of findings support the hypothesis that the unifying mechanism of action of ethanol in interference with glutamatergic neurotransmission, especially through the NMDA receptor, may be considered another member of the expanding family of glutamate-related neuropsychiatric disorders.

Reduced central serotonin transporters in alcoholism.

The hypothesis of serotonergic dysfunction in alcoholism and in withdrawal-emergent depressive symptoms is supported, which was significantly correlated with lifetime alcohol consumption and with ratings of depression and anxiety during withdrawal.