Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA.
Brain Cogn. 2010 Nov;74(2):132-44. doi: 10.1016/j.bandc.2010.07.013. Epub 2010 Aug 21.
Building on our previous neurocomputational models of basal ganglia and hippocampal region function (and their modulation by dopamine and acetylcholine, respectively), we show here how an integration of these models can inform our understanding of the interaction between the basal ganglia and hippocampal region in associative learning and transfer generalization across various patient populations. As a common test bed for exploring interactions between these brain regions and neuromodulators, we focus on the acquired equivalence task, an associative learning paradigm in which stimuli that have been associated with the same outcome acquire a functional similarity such that subsequent generalization between these stimuli increases. This task has been used to test cognitive dysfunction in various patient populations with damages to the hippocampal region and basal ganglia, including studies of patients with Parkinson's disease (PD), schizophrenia, basal forebrain amnesia, and hippocampal atrophy. Simulation results show that damage to the hippocampal region-as in patients with hippocampal atrophy (HA), hypoxia, mild Alzheimer's (AD), or schizophrenia-leads to intact associative learning but impaired transfer generalization performance. Moreover, the model demonstrates how PD and anterior communicating artery (ACoA) aneurysm-two very different brain disorders that affect different neural mechanisms-can have similar effects on acquired equivalence performance. In particular, the model shows that simulating a loss of dopamine function in the basal ganglia module (as in PD) leads to slow acquisition learning but intact transfer generalization. Similarly, the model shows that simulating the loss of acetylcholine in the hippocampal region (as in ACoA aneurysm) also results in slower acquisition learning. We argue from this that changes in associative learning of stimulus-action pathways (in the basal ganglia) or changes in the learning of stimulus representations (in the hippocampal region) can have similar functional effects.
基于我们之前关于基底神经节和海马区功能的神经计算模型（以及它们分别受多巴胺和乙酰胆碱的调节），我们在这里展示了如何整合这些模型，可以帮助我们理解基底神经节和海马区在联想学习和跨各种患者群体的转移泛化中的相互作用。作为探索这些大脑区域和神经调节剂之间相互作用的共同测试平台，我们专注于获得等价任务，这是一种联想学习范式，其中与相同结果相关联的刺激获得功能相似性，从而增加这些刺激之间的后续泛化。该任务已用于测试海马区和基底神经节受损的各种患者群体的认知功能障碍，包括帕金森病 (PD)、精神分裂症、基底前脑遗忘症和海马萎缩患者的研究。模拟结果表明，海马区受损（如海马萎缩 (HA)、缺氧、轻度阿尔茨海默病 (AD) 或精神分裂症患者）会导致完整的联想学习，但转移泛化表现受损。此外，该模型还展示了 PD 和前交通动脉瘤 (ACoA) 动脉瘤——两种影响不同神经机制的非常不同的大脑疾病——如何对获得等价性能产生相似的影响。特别是，该模型表明，模拟基底神经节模块中多巴胺功能丧失（如 PD 中）会导致学习速度变慢，但转移泛化正常。同样，该模型表明，模拟海马区乙酰胆碱丧失（如 ACoA 动脉瘤）也会导致学习速度变慢。我们由此认为，刺激-动作通路的联想学习变化（在基底神经节）或刺激表示的学习变化（在海马区）可能具有相似的功能影响。
