ASSOCIATIVE LEARNING IN BASAL FOREBRAIN AMNESIA

前交通动脉(ACOA)动脉瘤患者常表现为 顺行性遗忘综合征：形成新记忆的能力相对较差 但较旧的记忆相对较少(例如德卢卡和戴蒙德，1995)。 因此，ACOA健忘症从表面上看类似于随之而来的健忘症 损伤海马体及相关的内侧颞叶(MT)结构 (例如，乡绅，1987)，尽管ACOA赦免没有直接的MT伤害。 动物模型、药理学数据和计算模型表明 基底前脑结构调节海马体的处理，导致 ACoA遗忘症中的海马区处理中断(例如，Myers等人， 1996年)。然而，这些模型也预测了残差的细微差异。 基底前脑损伤后的记忆能力与MT损伤(例如，Myers 等人，1996年)。 这项工作建议测试一组ACOA健忘症(和适当的 匹配对照)在一系列这类联想学习任务上 已知的MT健忘症和海马区损害或幸免 动物。这些包括眨眼的运动反射条件反射。 反应和基于计算机的操作性条件反射任务。而简单 条件作用在MT健忘症中是不存在的，但更复杂的条件作用 如果涉及上下文或配置信息的信息受损，我们预计 在ACOA赦免中获得相反模式的结果。如果这个 预测，这些结果将代表区分 这两个群体的记忆力都有缺陷。这将通知当前 对正常人海马体和基底前脑相互作用的认识 记忆。此外，一系列对基本任务敏感的任务 前脑损害将有助于评估ACOA的损害范围 健忘症患者，对他们来说，神经成像通常是不确定的。最后，这一点 学习对接受过计算培训的PI来说是一个机会 内存系统建模，以获得新的经验和培训 通过与DeLuca博士和 戴蒙德，他有丰富的ACOA动脉瘤工作经验 幸存者和ACOA健忘症。

Patients with anterior communicating artery (ACoA) aneurysm often show an anterograde amnesia syndrome: relatively poor ability to form new memories but relative sparing of older memories (e.g., DeLuca and Diamond, 1995). ACoA amnesia is thus superficially similar to the amnesia which may follow damage to the hippocampus and associated medial temporal (MT) structure (e.g., Squire, 1987), although the ACoA amnesics have no direct MT damage. Animal models, pharmacological data, and computational models suggest that basal forebrain structures modulate hippocampal processing, leading to disrupted hippocampal processing in ACoA amnesia (e.g., Myers et al., 1996). However, these models also predict subtle differences in residual memory abilities following basal forebrain versus MT damage (e.g., Myers et al., 1996). This work proposes testing a population of ACoA amnesic (and appropriate matched controls) on a series of associative learning tasks of the kind known to be impaired or spared in MT amnesia and hippocampal-lesioned animals. These include motor-reflex conditioning of the eye-blink responses and computer-based operant conditioning tasks. Whereas simple conditioning is spared in MT amnesia, but more complex conditioning involving contextual or configural information is impaired, we expect the opposite pattern of results to obtain in the ACoA amnesics. If this prediction hods, these results will represent evidence differentiating the memory deficit in these two populations. This will inform current understanding of how hippocampus and basal forebrain interact in normal memory. Additionally, a battery of tasks which are sensitive to basal forebrain damage would be useful in a assessing lesion extent in ACoA amnesics, for whom neuroimaging is typically inconclusive. Finally, this study represents an opportunity for the PI, trained in computational modeling of memory systems, to gain new experience and training in clinical behavioral studies through collaboration with Drs. DeLuca and Diamond, who have extensive experience working with ACoA aneurysm survivors and ACoA amnesia.