Dopamine modulation of emotional processing in cortical and subcortical neural circuits: evidence for a final common pathway in schizophrenia?
The neural regulation of emotional perception, learning, and memory is essential for normal behavioral and cognitive functioning. Many of the symptoms displayed by individuals with schizophrenia may arise from fundamental disturbances in the ability to accurately process emotionally salient sensory information. The neurotransmitter dopamine (DA) and its ability to modulate neural regions involved in emotional learning, perception, and memory formation has received considerable research attention as a potential final common pathway to account for the aberrant emotional regulation and psychosis present in the schizophrenic syndrome. Evidence from both human neuroimaging studies and animal-based research using neurodevelopmental, behavioral, and electrophysiological techniques have implicated the mesocorticolimbic DA circuit as a crucial system for the encoding and expression of emotionally salient learning and memory formation. While many theories have examined the cortical-subcortical interactions between prefrontal cortical regions and subcortical DA substrates, many questions remain as to how DA may control emotional perception and learning and how disturbances linked to DA abnormalities may underlie the disturbed emotional processing in schizophrenia. Beyond the mesolimbic DA system, increasing evidence points to the amygdala-prefrontal cortical circuit as an important processor of emotionally salient information and how neurodevelopmental perturbances within this circuitry may lead to dysregulation of DAergic modulation of emotional processing and learning along this cortical-subcortical emotional processing circuit.
Laviolette
Steven R
SR
Dept of Anatomy & Cell Biology, The Schulich School of Medicine, University of Western Ontario, London, Ontario, Canada N6A 5C1. steven.laviolette@schulich.uwo.ca
D000339:Affect; D000679:Amygdala / Q000378:metabolism* / Q000503:physiopathology*; D003072:Cognition Disorders / Q000209:etiology*; D004298:Dopamine / Q000378:metabolism*; D006801:Humans; D007858:Learning / Q000502:physiology; D009042:Motivation; D009415:Nerve Net / Q000378:metabolism* / Q000503:physiopathology*; D009434:Neural Pathways / Q000378:metabolism* / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology; D017397:Prefrontal Cortex / Q000378:metabolism* / Q000503:physiopathology*; D012559:Schizophrenia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D017557:Ventral Tegmental Area / Q000378:metabolism* / Q000503:physiopathology*
D004298:Dopamine