The nucleus accumbens had been proposed as an anatomical substrate of limbic-motor integration. It gathers information from midbrain dopaminergic neurons that are activated by salient sensory stimuli and from glutamatergic afferents from the amydala, hippocampus and prefrontal cortex that encode memory of prior responses, the emotional state and the context. This information is processed and, based on previous learning, an appropriate motor response to the stimulus is generated.
We are particularly interested in the dopaminergic input to the nucleus accumbens. Midbrain dopaminergic neurons burst fire in response to natural reinforcers or to stimuli that have been paired to their delivery. This has been presumed to result in a subsecond, transient increase in dopamine in several forebrain structures. Recently, we confirmed this by making direct chemical measurements of such changes during presentation of natural reinforcers, drug reinforcers or their paired cues. Increases in forebrain dopamine typically result in motor activation. In particular, increases in dopamine in the nucleus accumbens have been implicated in goal-directed movements. Using cocaine self-administration as a model of drug abuse, we provided the first direct evidence that phasic dopamine changes are temporally linked to, and can trigger drug-seeking behavior.
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Fred Hutchison Cancer Research Center | University of Washington
Institute for Systems Biology | Seattle Biomed