D'Souza Manoranjan S, Markou Athina
Department of Psychiatry, University of California, San Diego, La Jolla, CA 92093, USA.
Curr Top Behav Neurosci. 2010;3:119-78. doi: 10.1007/7854_2009_20.
Psychostimulant drugs have powerful reinforcing and hedonic properties and are frequently abused. Cessation of psychostimulant administration results in a withdrawal syndrome characterized by anhedonia (i.e., an inability to experience pleasure). In humans, psychostimulant withdrawal-induced anhedonia can be debilitating and has been hypothesized to play an important role in relapse to drug use. Hence, understanding the neural substrates involved in psychostimulant withdrawal-induced anhedonia is essential. In this review, we first summarize the theoretical perspectives of psychostimulant withdrawal-induced anhedonia. Experimental procedures and measures used to assess anhedonia in experimental animals are also discussed. The review then focuses on neural substrates hypothesized to play an important role in anhedonia experienced after termination of psychostimulant administration, such as with cocaine, amphetamine-like drugs, and nicotine. Both neural substrates that have been extensively investigated and some that need further evaluation with respect to psychostimulant withdrawal-induced anhedonia are reviewed. In the context of reviewing the various neurosubstrates of psychostimulant withdrawal, we also discuss pharmacological medications that have been used to treat psychostimulant withdrawal in humans. This literature review indicates that great progress has been made in understanding the neural substrates of anhedonia associated with psychostimulant withdrawal. These advances in our understanding of the neurobiology of anhedonia may also shed light on the neurobiology of nondrug-induced anhedonia, such as that seen as a core symptom of depression and a negative symptom of schizophrenia.
精神刺激药物具有强大的强化和享乐特性，且常被滥用。停止使用精神刺激药物会导致一种戒断综合征，其特征为快感缺失（即无法体验愉悦）。在人类中，精神刺激药物戒断引发的快感缺失可能使人衰弱，并被认为在药物使用复发中起重要作用。因此，了解精神刺激药物戒断引发快感缺失所涉及的神经基质至关重要。在本综述中，我们首先总结精神刺激药物戒断引发快感缺失的理论观点。还将讨论用于评估实验动物快感缺失的实验程序和测量方法。然后，综述聚焦于被认为在停止使用精神刺激药物（如可卡因、苯丙胺类药物和尼古丁）后所体验到的快感缺失中起重要作用的神经基质。我们将综述已被广泛研究的神经基质以及一些在精神刺激药物戒断引发快感缺失方面需要进一步评估的神经基质。在回顾精神刺激药物戒断的各种神经基质的背景下，我们还将讨论已用于治疗人类精神刺激药物戒断的药物。这篇文献综述表明，在理解与精神刺激药物戒断相关的快感缺失的神经基质方面已取得了很大进展。我们对快感缺失神经生物学的这些认识进展也可能为非药物诱导的快感缺失（如作为抑郁症的核心症状和精神分裂症的阴性症状所见）的神经生物学提供启示。
