Dackis C A, Gold M S
Neurosci Biobehav Rev. 1985 Fall;9(3):469-77. doi: 10.1016/0149-7634(85)90022-3.
Euphoric properties of cocaine lead to the development of chronic abuse, and appear to involve the acute activation of central DA neuronal systems. This is based upon known effects of cocaine on DA neurons, and the role played by DA in reward states and self-stimulation behavior. With chronic cocaine use, neurotransmitter and neuroendocrine alterations occur. DA depletion is hypothesized to result from overstimulation of these neurons and excessive synaptic metabolism of the neurotransmitter. DA depletion may underlie dysphoric aspects of cocaine abstinence, and cocaine urges. Neurochemical disruptions caused by cocaine are consistent with the concept of "physical" rather than "psychological" addiction. Possible pharmacological interventions in cocaine addiction are outlined and the psychological approach to these patients is discussed.
可卡因的欣快特性会导致慢性滥用的形成，且似乎涉及中枢多巴胺（DA）神经元系统的急性激活。这是基于可卡因对多巴胺能神经元的已知作用，以及多巴胺在奖赏状态和自我刺激行为中所起的作用。长期使用可卡因会导致神经递质和神经内分泌改变。据推测，多巴胺耗竭是这些神经元过度刺激以及神经递质突触代谢过度所致。多巴胺耗竭可能是可卡因戒断时烦躁不安和渴望可卡因的潜在原因。可卡因引起的神经化学紊乱与“生理”而非“心理”成瘾的概念相符。文中概述了针对可卡因成瘾可能的药物干预措施，并讨论了针对这些患者的心理治疗方法。
