University of Melbourne, School of Psychological Sciences, Melbourne, Victoria, Australia.
University of Melbourne, School of Psychological Sciences, Melbourne, Victoria, Australia; Graeme Clark Institute for Biomedical Engineering, Melbourne, Victoria, Australia.
Neural Netw. 2023 Nov;168:631-650. doi: 10.1016/j.neunet.2023.09.032. Epub 2023 Sep 25.
Dysfunction in learning and motivational systems are thought to contribute to addictive behaviours. Previous models have suggested that dopaminergic roles in learning and motivation could produce addictive behaviours through pharmacological manipulations that provide excess dopaminergic signalling towards these learning and motivational systems. Redish (2004) suggested a role based on dopaminergic signals of value prediction error, while (Zhang et al., 2009) suggested a role based on dopaminergic signals of motivation. However, both models present significant limitations. They do not explain the reduced sensitivity to drug-related costs/negative consequences, the increased impulsivity generally found in people with a substance use disorder, craving behaviours, and non-pharmacological dependence, all of which are key hallmarks of addictive behaviours. Here, we propose a novel mathematical definition of salience, that combines aspects of dopamine's role in both learning and motivation within the reinforcement learning framework. Using a single parameter regime, we simulated addictive behaviours that the (Zhang et al., 2009; Redish, 2004) models also produce but we went further in simulating the downweighting of drug-related negative prediction-errors, steeper delay discounting of drug rewards, craving behaviours and aspects of behavioural/non-pharmacological addictions. The current salience model builds on our recently proposed conceptual theory that salience modulates internal representation updating and may contribute to addictive behaviours by producing misaligned internal representations (Kalhan et al., 2021). Critically, our current mathematical model of salience argues that the seemingly disparate learning and motivational aspects of dopaminergic functioning may interact through a salience mechanism that modulates internal representation updating.
学习和动机系统的功能障碍被认为是导致成瘾行为的原因。以前的模型表明,通过提供对这些学习和动机系统的过度多巴胺信号的药理学操作,多巴胺能在学习和动机中的作用可能产生成瘾行为。Redish(2004)提出了基于多巴胺信号价值预测误差的作用,而(Zhang 等人,2009)提出了基于多巴胺信号动机的作用。然而,这两种模型都存在显著的局限性。它们不能解释对与药物相关的成本/负面后果的敏感性降低、在物质使用障碍患者中普遍发现的冲动性增加、渴望行为以及非药物依赖,所有这些都是成瘾行为的关键特征。在这里,我们提出了一个新颖的突显数学定义,该定义将多巴胺在学习和动机中的作用结合在强化学习框架内。使用单个参数状态,我们模拟了(Zhang 等人,2009;Redish,2004)模型也产生的成瘾行为,但我们更进一步模拟了对与药物相关的负面预测误差的权重降低、药物奖励的延迟折扣更陡峭、渴望行为以及行为/非药物成瘾的各个方面。当前的显着性模型建立在我们最近提出的概念理论之上,即显着性调节内部表示更新,并且通过产生不匹配的内部表示可能导致成瘾行为(Kalhan 等人,2021)。至关重要的是,我们当前的多巴胺能突显数学模型认为,多巴胺能功能的看似不同的学习和动机方面可能通过调节内部表示更新的突显机制相互作用。