Striatal dopamine (DA) is increased by virtually all drugs of abuse, including alcohol. However, drug-associated cues are also known to provoke striatal DA transmission- a phenomenon linked to the motivated behaviors associated with addiction. To our knowledge, no one has tested if alcohol’s classically-conditioned flavor cues, in the absence of a significant pharmacologic effect, are capable of eliciting striatal dopamine release in humans.
Employing positron emission tomography (PET), we hypothesized that beer’s flavor alone can reduce the binding potential of [11C]raclopride (a reflection of striatal DA release) in the ventral striatum, relative to an appetitive flavor control.
Forty-nine men, ranging from social to heavy drinking, mean age 25, with a varied family history of alcoholism underwent two [11C]raclopride PET scans: one while tasting beer, and one while tasting Gatorade®.
Relative to the control flavor of Gatorade, beer flavor significantly increased self-reported desire to drink, and reduced [11C]raclopride binding potential, indicating that the alcohol-associated flavor cues induced dopamine release.
Binding potential reductions were strongest in subjects with first-degree alcoholic relatives. These results demonstrate that alcohol-conditioned flavor cues can provoke ventral striatal dopamine release absent significant pharmacologic effects, and that the response is strongest in subjects with a greater genetic risk for alcoholism.
Striatal DA responses to salient alcohol cues may thus be an inherited risk factor for alcoholism.
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