Department of Psychiatry, Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, New York; Department of Radiology, Columbia University College of Physicians and Surgeons, New York, New York.
Department of Psychiatry, Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, New York.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2018 Jul;3(7):591-598. doi: 10.1016/j.bpsc.2018.03.018. Epub 2018 Apr 21.
We used positron emission tomography imaging with [C]raclopride to examine the effects of consumption of alcohol or placebo beverage by participants with alcohol use disorder (AUD) compared with healthy participants with and without family history of AUD. We sought to assess dopamine release following alcohol exposure in relation to AUD risk.
Three groups were enrolled: participants with AUD (n = 15) and healthy participants with family history negative (n = 34) or positive (n = 16) for AUD. Participants consumed a placebo (n = 65) or alcohol (n = 63) beverage in counterbalanced order before positron emission tomography scanning (128 scans). Binding potential (BP) in the two drink conditions and the percent change in BP between conditions were evaluated across striatal subregions. Subjective effects of beverage consumption were rated. Effects of group, drink order, and sex were evaluated.
Alcohol resulted in greater dopamine release than did placebo in the ventral striatum (p < .001). There were no main effects of group, drink order, or sex on ventral striatum BP or percent change in BP. However, there was a drink order-by-group interaction (p = .02) whereby family history-positive participants who received placebo first had both lower placebo BP and less difference between placebo and alcohol BP than all other groups, consistent with expectation of alcohol powerfully evoking dopamine release in this group. Subjective responses showed the same order-by-group interaction.
Hyper-responsivity of the dopaminergic system in family history-positive participants to expectation of alcohol may contribute to the expression of familial risk for AUD.
我们使用 [C]raclopride 正电子发射断层扫描成像来检查酒精使用障碍 (AUD) 患者与健康参与者(无论是否有 AUD 家族史)在饮用酒精或安慰剂饮料后的影响。我们试图评估酒精暴露后与 AUD 风险相关的多巴胺释放。
共纳入三组参与者:AUD 患者(n=15)和 AUD 家族史阴性(n=34)或阳性(n=16)的健康参与者。参与者在正电子发射断层扫描(共 128 次扫描)前以平衡方式饮用安慰剂(n=65)或酒精(n=63)饮料。评估了两个饮料条件下纹状体亚区的结合潜力 (BP) 和条件之间 BP 的百分比变化。评定了饮料消费的主观效应。评估了组、饮料顺序和性别的影响。
与安慰剂相比,酒精在腹侧纹状体中导致更大的多巴胺释放(p<.001)。组、饮料顺序或性别对腹侧纹状体 BP 或 BP 百分比变化均无主要影响。然而,存在饮料顺序-组相互作用(p=0.02),即首先接受安慰剂的家族史阳性参与者的安慰剂 BP 较低,且安慰剂和酒精 BP 之间的差异小于其他所有组,这与预期的酒精在该组中强烈引发多巴胺释放一致。主观反应也表现出相同的顺序-组相互作用。
家族史阳性参与者对酒精的期待引起的多巴胺系统超反应性可能导致 AUD 的家族风险表达。