ASSOCIATIVE LEARNING IN BASAL FOREBRAIN AMNESIA

前交通动脉（ACoA）动脉瘤患者通常表现为 顺行性遗忘综合征：形成新记忆的能力相对较差 但是相对保留较旧的存储器（例如，DeLuca和Diamond，1995年）。 因此，前交通动脉失忆症与随后可能出现的失忆症在表面上相似。 海马和相关内侧颞叶（MT）结构的损伤 (e.g., Squire，1987），尽管ACoA遗忘者没有直接的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处理，导致 在ACoA健忘症中破坏海马体加工（例如，Myers等人， 1996年）。然而，这些模型也预测残差的细微差异， 基底前脑损伤后的记忆能力与MT损伤（例如，迈尔斯 例如，1996年）。 这项工作提出了测试人口的ACoA健忘症（和适当的 匹配的控制）的一系列联想学习任务的种类 已知在MT健忘症和脑血管病变中受损或幸免 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。虽然简单 条件反射在MT健忘症中是不存在的，但更复杂的条件反射 涉及上下文或结构信息受损，我们预计 在ACoA健忘症中获得的结果相反。如果这 预测hods，这些结果将代表区分 这两个群体的记忆力都有缺陷这将告知当前 了解海马和基底前脑在正常情况下如何相互作用 记忆此外，一系列对基础胰岛素敏感的任务 前脑损伤将有助于评估ACoA的病变程度 健忘症患者，对他们来说，神经成像通常是不确定的。最后 研究为PI提供了一个机会， 记忆系统建模，以获得新的经验和培训， 通过与DeLuca博士合作进行临床行为研究， Diamond在ACoA动脉瘤治疗方面有丰富的经验， 幸存者和大脑前交通动脉失忆症

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.