Repeated drug use can change dopamine (DA) function in ways that promote the development and persistence of addiction, but in what direction? By one view, drug use blunts DA neurotransmission, producing a hypodopaminergic state that fosters further drug use to overcome a DA deficiency. Another view is that drug use enhances DA neurotransmission, producing a sensitized, hyperdopaminergic reaction to drugs and drug cues. According to this second view, continued drug use is motivated by sensitization of drug ‘wanting’. Here we discuss recent evidence supporting the latter view, both from preclinical studies using intermittent cocaine self-administration procedures that mimic human patterns of use and from related human neuroimaging studies. These studies have implications for the modeling of addiction in the laboratory and for treatment.

反复吸毒可以改变多巴胺 (DA) 的功能，从而促进成瘾的发展和持续存在，但方向是什么？一种观点认为，药物使用会削弱 DA 神经传递，产生一种低多巴胺能状态，从而促进进一步的药物使用以克服 DA 缺乏症。另一种观点是，药物使用增强了 DA 神经传递，对药物和药物线索产生敏感的多巴胺能反应。根据第二种观点，继续吸毒的动机是对药物“想要”的敏感性。在这里，我们讨论了支持后一种观点的最新证据，这些证据来自使用模拟人类使用模式的间歇性可卡因自我给药程序的临床前研究和相关的人类神经影像学研究。这些研究对实验室中成瘾的建模和治疗具有影响。