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A summary of the Third International Obsessive Compulsive Disorder Conference proceedings on neuroimaging research and neurocircuitry models of obsessive-compulsive disorder (OCD) is presented. This survey of recent and ongoing research indicates that a wide range of modern techniques and experimental strategies are being employed in a complementary fashion to enhance our understanding of OCD. Imaging studies in animal models of OCD are helping to elaborate relevant normal anatomy and neuro-chemistry. Functional imaging methods are being employed in conjunction with behavioral, pharmacologic, and cognitive challenge paradigms. Magnetic resonance spectroscopy as well as radiotracer methods are being utilized to measure neurochemical and neuropharmacologic indices in OCD. Transcranial magnetic stimulation has emerged as a tool for probing neurocircuitry that may also have therapeutic potential. Experimental designs and data-analytic methods are evolving to help elucidate the pathophysiology of OCD and related disorders, delineate neurobiologically meaningful subtypes of OCD, and identify potential predictors of treatment response. Collectively, these efforts promise important advances as we approach the new millennium.
Low serotonin transmission is thought to increase susceptibility to a wide range of substance use disorders and impulsive traits.
Aims
To investigate the effects of lowered serotonin on cocaine-induced (1.0 mg/kg cocaine, self-administered intranasally) dopamine responses and drug craving.
Method
In non-dependent cocaine users, serotonin transmission was reduced using the acute tryptophan depletion method. Striatal dopamine responses were measured using positron emission tomography with [11C]raclopride.
Results
Acute tryptophan depletion increased drug craving and striatal dopamine responses to cocaine. These acute tryptophan depletion-induced increases did not occur in the absence of cocaine.
Conclusions
The results suggest that low serotonin transmission can increase dopaminergic and appetitive responses to cocaine. These findings might identify a mechanism by which individuals with low serotonin are at elevated risk for both substance use disorders and comorbid conditions.
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