Combining Stress and Dopamine Based Models of Addiction: Towards a Psycho-Neuro-Endocrinological Theory of Addiction.

James H. Johnston, D. Linden, M. V. D. van den Bree
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引用次数: 27

Abstract

The literature on the two main models of addiction (dopamine-based positive reinforcement and stress-based negative reinforcement models) have made many important contributions to understanding this brain disorder. However, rarely has there been a comprehensive critique of the limitations of both models. This article seeks to resolve theoretical issues inherent to each model, as well as propose a more comprehensive psycho-neuro-endocrinological theory of addiction which reconciles important elements of both. We suggest that there is not only direct interaction of dopaminergic and stress systems throughout the addiction cycle, from initial use, via the abusing stage, to the endpoint of addiction, but that this interaction is present prior to initial use. A combination of genetic factors and/or experiences of adversity may result in a stress-triggered sensitisation of dopaminergic networks which is present before the onset of substance use, which cannot be explained solely in terms of dopaminergic (positive) reinforcement. Rather these processes are best explained by an allostatic model which reconciles aspects of both models of addiction and shows how dopamine/stress interactions become increasingly pathological in the addiction cycle. Our model suggests that chronic stress eventually creates baseline hypodopaminergic activity, but also prompts dopaminergic hyperactivity in cue reactivity. This is the neural marker of allostatic mechanisms observed at endpoint addiction. We propose a multi-circuit explanation of how this cumulative effect of stress increasingly impacts on dopaminergic networks of reward, affect, attention, memory and behavioural control. This revised model provides a useful frame of reference for further research and ultimately clinical practice.
结合压力和多巴胺成瘾模型:迈向成瘾的心理-神经-内分泌学理论。
关于成瘾的两种主要模型(基于多巴胺的正强化模型和基于压力的负强化模型)的文献对理解这种大脑疾病做出了许多重要贡献。然而,很少有人对这两种模型的局限性进行全面的批评。本文试图解决每个模型固有的理论问题,并提出一个更全面的成瘾心理-神经-内分泌理论,以调和两者的重要因素。我们认为,在整个成瘾周期中,从最初的使用,通过滥用阶段,到成瘾的终点,不仅存在多巴胺能和压力系统的直接相互作用,而且这种相互作用在最初使用之前就存在。遗传因素和/或逆境经历的结合可能导致在物质使用开始之前就存在的压力触发的多巴胺能网络敏化,这不能仅仅从多巴胺能(正)强化的角度来解释。相反,这些过程最好通过适应模型来解释,该模型调和了成瘾模型的两个方面,并显示了多巴胺/压力相互作用如何在成瘾周期中变得越来越病态。我们的模型表明,慢性压力最终会产生基线低多巴胺能活动,但也会在线索反应中促使多巴胺能过度活跃。这是在终点成瘾中观察到的适应机制的神经标志。我们提出了一种多回路的解释,解释压力的累积效应如何越来越多地影响多巴胺能网络的奖励、影响、注意、记忆和行为控制。这个修正后的模型为进一步的研究和最终的临床实践提供了有用的参考框架。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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