Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA.
J Cogn Neurosci. 2011 Jan;23(1):151-67. doi: 10.1162/jocn.2010.21420.
Most existing models of dopamine and learning in Parkinson disease (PD) focus on simulating the role of basal ganglia dopamine in reinforcement learning. Much data argue, however, for a critical role for prefrontal cortex (PFC) dopamine in stimulus selection in attentional learning. Here, we present a new computational model that simulates performance in multicue category learning, such as the "weather prediction" task. The model addresses how PD and dopamine medications affect stimulus selection processes, which mediate reinforcement learning. In this model, PFC dopamine is key for attentional learning, whereas basal ganglia dopamine, consistent with other models, is key for reinforcement and motor learning. The model assumes that competitive dynamics among PFC neurons is the neural mechanism underlying stimulus selection with limited attentional resources, whereas competitive dynamics among striatal neurons is the neural mechanism underlying action selection. According to our model, PD is associated with decreased phasic and tonic dopamine levels in both PFC and basal ganglia. We assume that dopamine medications increase dopamine levels in both the basal ganglia and PFC, which, in turn, increase tonic dopamine levels but decrease the magnitude of phasic dopamine signaling in these brain structures. Increase of tonic dopamine levels in the simulated PFC enhances attentional shifting performance. The model provides a mechanistic account for several phenomena, including (a) medicated PD patients are more impaired at multicue probabilistic category learning than unmedicated patients and (b) medicated PD patients opt out of reversal when there are alternative and redundant cue dimensions.
大多数现有的帕金森病(PD)多巴胺和学习模型都侧重于模拟基底神经节多巴胺在强化学习中的作用。然而,大量数据表明,前额叶皮层(PFC)多巴胺在注意力学习中的刺激选择中起着关键作用。在这里,我们提出了一个新的计算模型,该模型模拟了多线索类别学习的性能,例如“天气预报”任务。该模型解决了 PD 和多巴胺药物如何影响刺激选择过程,从而影响强化学习。在这个模型中,PFC 多巴胺是注意力学习的关键,而基底神经节多巴胺与其他模型一致,是强化和运动学习的关键。该模型假设 PFC 神经元之间的竞争动力学是在有限的注意力资源下进行刺激选择的神经机制,而纹状体神经元之间的竞争动力学是进行动作选择的神经机制。根据我们的模型,PD 与 PFC 和基底神经节中相位和紧张性多巴胺水平降低有关。我们假设多巴胺药物会增加基底神经节和 PFC 中的多巴胺水平,这反过来又会增加这些脑结构中的紧张性多巴胺水平,但会降低相位多巴胺信号的幅度。模拟 PFC 中紧张性多巴胺水平的升高增强了注意力转移表现。该模型为几种现象提供了一种机制解释,包括:(a)接受药物治疗的 PD 患者在多线索概率类别学习方面比未接受药物治疗的患者受损更严重;(b)当存在替代和冗余的线索维度时,接受药物治疗的 PD 患者会选择退出反转。