Dissociating hippocampal versus basal ganglia contributions to learning and transfer
Dissociating hippocampal versus basal ganglia contributions to learning and transfer
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DOI：
10.1162/089892903321208123
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发表时间：
2003-02-01
影响因子：
3.2
通讯作者：
Schwartz, R
中科院分区：
文献类型：
--
作者：
Myers, CE;Shohamy, D;Schwartz, R
基于先前的动物和计算模型，我们提出在内侧颞叶（海马）损伤患者与帕金森病（基底神经节功能障碍）患者中观察到的联想学习缺陷之间存在双重分离。具体来说，我们预计基底神经节功能障碍可能会导致学习速度减慢，而海马损伤的个体可能会以正常速度学习。然而，当面临转移任务时，以前学到的信息以新的重组形式呈现，我们预计海马损伤会损害泛化，但基底神经节功能障碍不会。我们使用“获得对等”联想学习任务，在一组患有轻度至中度海马萎缩的健康老年人、一组患有轻度帕金森病的患者和健康对照组中测试了这一预测。正如预测的那样，帕金森病患者的初始学习速度较慢，但随后迁移良好，而海马萎缩组则表现出相反的模式：初始学习良好，但迁移受损。据我们所知，这是第一次使用单个任务来证明海马与基底神经节损伤/功能障碍引起的联想学习障碍之间的双重分离。这一发现对于理解内侧颞叶和基底神经节对学习和记忆的独特贡献具有重要意义。
Based on prior animal and computational models, we propose a double dissociation between the associative learning deficits observed in patients with medial temporal (hippocampal) damage versus patients with Parkinson's disease (basal ganglia dysfunction). Specifically, we expect that basal ganglia dysfunction may result in slowed learning, while individuals with hippocampal damage may learn at normal speed. However, when challenged with a transfer task where previously learned information is presented in novel recombinations, we expect that hippocampal damage will impair generalization but basal ganglia dysfunction will not. We tested this prediction in a group of healthy elderly with mild-to-moderate hippocampal atrophy, a group of patients with mild Parkinson's disease, and healthy controls, using an "acquired equivalence" associative learning task. As predicted, Parkinson's patients were slower on the initial learning but then transferred well, while the hippocampal atrophy group showed the opposite pattern: good initial learning with impaired transfer. To our knowledge, this is the first time that a single task has been used to demonstrate a double dissociation between the associative learning impairments caused by hippocampal versus basal ganglia damage/dysfunction. This finding has implications for understanding the distinct contributions of the medial temporal lobe and basal ganglia to learning and memory.