A neural model of normal and abnormal learning and memory consolidation: adaptively timed conditioning, hippocampus, amnesia, neurotrophins, and consciousness

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• 作者：Daniel J. Franklin ; Stephen Grossberg
• 关键词：Cognitive ; emotional learning ; Conditioning ; Memory consolidation ; Amnesia ; Hippocampus ; Amygdala ; Pontine nuclei ; Adaptive timing ; Time cells ; BDNF
• 刊名：Cognitive, Affective, & Behavioral Neuroscience
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：17
• 期：1
• 页码：24-76
• 全文大小：4432KB
• 刊物主题：Cognitive Psychology; Neurosciences;
• 出版者：Springer US
• ISSN：1531-135X
• 卷排序：17

文摘

How do the hippocampus and amygdala interact with thalamocortical systems to regulate cognitive and cognitive-emotional learning? Why do lesions of thalamus, amygdala, hippocampus, and cortex have differential effects depending on the phase of learning when they occur? In particular, why is the hippocampus typically needed for trace conditioning, but not delay conditioning, and what do the exceptions reveal? Why do amygdala lesions made before or immediately after training decelerate conditioning while those made later do not? Why do thalamic or sensory cortical lesions degrade trace conditioning more than delay conditioning? Why do hippocampal lesions during trace conditioning experiments degrade recent but not temporally remote learning? Why do orbitofrontal cortical lesions degrade temporally remote but not recent or post-lesion learning? How is temporally graded amnesia caused by ablation of prefrontal cortex after memory consolidation? How are attention and consciousness linked during conditioning? How do neurotrophins, notably brain-derived neurotrophic factor (BDNF), influence memory formation and consolidation? Is there a common output path for learned performance? A neural model proposes a unified answer to these questions that overcome problems of alternative memory models.