Binge alcohol use is not associated with alterations in striatal dopamine receptor binding or dopamine release.
case_control · Level III
Where this comes from
- Record sourced from PubMed, PMID 31669800.
- Also identified by DOI 10.1016/j.drugalcdep.2019.107627 and PMC identifier 6893096.
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Abstract
Previous imaging studies using Positron Emission Tomography (PET) have shown that alcohol use disorder (AUD) is associated with a decrease in dopamine type 2/3 receptor (D<sub>2/3</sub>) binding and dopamine transmission. Although binge drinking is a risk factor for future AUD, little is known about the neurobiology of binge drinking in young adults. This study measured D<sub>2/3</sub> receptor binding and stimulant-induced dopamine release using PET and [<sup>11</sup>C]raclopride in binge drinkers without an AUD. This study included 14 healthy controls (HC) and 14 young adult binge drinkers (BD), aged 18-25. The BD met National Institute on Alcohol Abuse and Alcoholism (NIAAA) criteria for binge drinking and the HC subjects were social drinkers. The subjects were scanned with [<sup>11</sup>C]raclopride before and after the administration of oral methylphenidate (60 mg) to measure D<sub>2/3</sub> binding and dopamine release. There was no significant difference in the PET measures of D<sub>2/3</sub> binding or methylphenidate-induced dopamine release between the two groups. There was no significant association between Alcohol Use Disorders Identification Test (AUDIT) scores or 30-day drinking history and the imaging data. In this sample of 18-25-year-old binge drinkers without a diagnosis of a substance use disorder, there were no significant differences in D<sub>2/3</sub> receptor binding potential or methylphenidate-induced dopamine release relative to healthy controls.
Medical subject headings
- Binge Drinking
- Corpus Striatum
- Dopamine
- Ethanol
- Receptors, Dopamine D2
- Receptors, Dopamine D3