Improvement of Brain Reward Abnormalities by Antipsychotic Monotherapy in Schizophrenia

Abstract

Dopamine is an essential neurotransmitter in the brain reward system^1,2 and dopaminergic dysfunction has been suggested to be involved in the development of psychotic symptoms.³ A dysregulated hyperdopaminergic state in the striatum might lead to development of psychoses through altered reward processing,^4,5 and antipsychotic medication is thought to relieve the psychotic symptoms by normalizing this altered transmission via D₂ antagonism.⁶ As a result, studies of reward processing in schizophrenia are of considerable interest, and studies in unmedicated patients consistently find an attenuated signal in the ventral striatum (VS) during reward anticipation.^7,8 This has been suggested to be a result of an increased tonic dopaminergic tone that increases the noise, thereby decreasing the signal to noise ratio. Thus, the event-related blood oxygen level–dependent (BOLD) responses are often smaller, because phasic dopamine responses may not sufficiently differentiate from tonic dopamine levels.⁹