Abstract
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 DA release in humans.
Employing positron emission tomography (PET), we hypothesized that
beer's flavor alone can reduce the binding potential (BP) of [(11)C]raclopride
(RAC; 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 [(11)C]RAC 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 [(11)C]RAC BP,
indicating that the alcohol-associated flavor cues induced DA release.
BP reductions were strongest in subjects with first-degree alcoholic relatives.
These results demonstrate that alcohol-conditioned flavor cues
can provoke ventral striatal DA 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.
