NEURAL BASIS OF SERIAL-PATTERN LEARNING IN RATS

这项研究计划的长期目标是开发一种 机械记忆和规则学习的一般心理生物学模型 大鼠序列模式学习的过程。 最近的研究结果表明 海马结构与记忆密切相关 序列模式学习，而大脑的其他结构， 特别是前额叶皮层，可能介导认知 “组块”过程。 该研究提出了两个具体的 目标。 第一个目的是进一步探讨串行的想法， 模式学习通过至少两个学习/记忆来实现 系统，即死记硬背和规则学习系统。 第二个目的 是开始探索认知的神经基础 大鼠序列模式学习中的“组块”过程。 这些目标 将通过测试死记硬背和规则的概念来完成， 学习过程可能会因大脑皮层受损而分离。 海马结构，并通过测试的概念，损害 前额叶皮层导致“组块”过程的中断。 研究将集中在使用已建立的串行模式学习 测试证明海马损伤的影响， 前额叶皮层对序列模式学习过程的影响。 这些研究将扩展我们对两者的理解。 认知动物的学习和记忆过程， 这些过程的神经生物学基础。 这 方法提供了一个潜在的重新接近目前 冲突死记硬背和规则为基础的顺序学习模型， 区分和表征不同的神经基质 支持这些进程。 这样的模型也具有一般性。 认知和行为功能障碍模型的意义 导致的神经系统疾病

The long-term goal of this research program is to develop a general psychobiological model of rote- and rule-learning processes in rat serial-pattern learning. Recent findings suggest that the hippocampal formation is intimately involved in rote serial-pattern learning, whereas other structures of the brain, especially the prefrontal cortex, may mediate cognitive "chunking" processes. The proposed research has two specific aims. The first aim is to further explore the idea that serial pattern learning is subserved by at least two learning/memory systems, namely rote- and rule-learning systems. The second aim is to begin to explore the neural substrates of cognitive "chunking" processes in rat serial-pattern learning. These aims will be accomplished by testing the notion that rote- and rule- learning processes can be dissociated by damage to the hippocampal formation, and by testing the notion that damage to prefrontal cortex results in disruptions of "chunking" processes. The reseach will focus on using established serial-pattern-learning tests to demonstrate the effects of lesioning hippocampus and prefrontal cortex on serial-pattern learning processes. These lines of research will extend our understanding of both cognitive animal learning and memory processes and the neurobiological basis of these processes in the rat brain. This approach offers a potential reapproachment of currently conflicting rote- and rule-based models of sequential learning by distinguishing and characterizing the separate neural substrates subserving these processes. Such a model would also have general implications for models of cognitive and behavioral dysfunction resulting from neurological disorders.