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dc.contributor.authorFranklin, Daniel Jonen_US
dc.date.accessioned2016-12-19T19:21:18Z
dc.date.available2016-12-19T19:21:18Z
dc.date.issued2016
dc.identifier.urihttps://hdl.handle.net/2144/19722
dc.description.abstractThe amygdala and hippocampus interact with thalamocortical systems to regulate cognitive-emotional learning, and lesions of amygdala, hippocampus, thalamus, and cortex have different effects depending on the phase of learning when they occur. In examining eyeblink conditioning data, several questions arise: Why is the hippocampus needed for trace conditioning where there is a temporal gap between the conditioned stimulus offset and the onset of the unconditioned stimulus, but not needed for delay conditioning where stimuli temporally overlap and co-terminate? Why do amygdala lesions made before or immediately after training decelerate conditioning while those made later have no impact on conditioned behavior? Why do thalamic lesions degrade trace conditioning more than delay conditioning? Why do hippocampal lesions degrade recent learning but not temporally remote learning? Why do cortical lesions degrade temporally remote learning, and cause amnesia, but not recent or post-lesion learning? How is temporally graded amnesia caused by ablation of medial prefrontal cortex? How are mechanisms of motivated attention and the emergent state of consciousness linked during conditioning? How do neurotrophins, notably Brain Derived Neurotrophic Factor (BDNF), influence memory formation and consolidation? A neural model, called neurotrophic START, or nSTART, proposes answers to these questions. The nSTART model synthesizes and extends key principles, mechanisms, and properties of three previously published brain models of normal behavior. These three models describe aspects of how the brain can learn to categorize objects and events in the world; how the brain can learn the emotional meanings of such events, notably rewarding and punishing events, through cognitive-emotional interactions; and how the brain can learn to adaptively time attention paid to motivationally important events, and when to respond to these events, in a context-appropriate manner. The model clarifies how hippocampal adaptive timing mechanisms and BDNF may bridge the gap between stimuli during trace conditioning and thereby allow thalamocortical and corticocortical learning to take place and be consolidated. The simulated data arise as emergent properties of several brain regions interacting together. The model overcomes problems of alternative memory models, notably models wherein memories that are initially stored in hippocampus move to the neocortex during consolidation.en_US
dc.language.isoen_US
dc.rightsAttribution 4.0 Internationalen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectNeurosciencesen_US
dc.subjectBDNFen_US
dc.subjectAdaptive timingen_US
dc.subjectConditioningen_US
dc.subjectHippocampusen_US
dc.subjectMotivationen_US
dc.subjectOrbitofrontal cortexen_US
dc.titleA neural network model of normal and abnormal learning and memory consolidationen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-12-04T02:06:51Z
etd.degree.nameDoctor of Philosophyen_US
etd.degree.leveldoctoralen_US
etd.degree.disciplineCognitive & Neural Systemsen_US
etd.degree.grantorBoston Universityen_US


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International