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dc.contributor.authorHerzallah, Mohammed
dc.contributor.authorMoustafa, Ahmed
dc.contributor.authorKeri, Szabolcs
dc.contributor.authorMyers, Catherine
dc.contributor.authorGluck, Mark
dc.date.accessioned2018-08-16T04:25:22Z
dc.date.available2018-08-16T04:25:22Z
dc.date.issued2010-08-21
dc.identifier.issn0278-2626
dc.identifier.urihttps://dspace.alquds.edu/handle/20.500.12213/739
dc.description.abstractBuilding on our previous neurocomputational models of basal ganglia and hippocampal region function (and their modulation by dopamine and acetylcholine, respectively), we show here how an integration of these models can inform our understanding of the interaction between the basal ganglia and hippocampal region in associative learning and transfer generalization across various patient populations. As a common test bed for exploring interactions between these brain regions and neuromodulators, we focus on the acquired equivalence task, an associative learning paradigm in which stimuli that have been associated with the same outcome acquire a functional similarity such that subsequent generalization between these stimuli increases. This task has been used to test cognitive dysfunction in various patient populations with damages to the hippocampal region and basal ganglia, including studies of patients with Parkinson’s disease (PD), schizophrenia, basal forebrain amnesia, and hippocampal atrophy. Simulation results show that damage to the hippocampal region—as in patients with hippocampal atrophy (HA), hypoxia, mild Alzheimer’s (AD), or schizophrenia—leads to intact associative learning but impaired transfer generalization performance. Moreover, the model demonstrates how PD and anterior communicating artery (ACoA) aneurysm—two very different brain disorders that affect different neural mechanisms— can have similar effects on acquired equivalence performance. In particular, the model shows that simulating a loss of dopamine function in the basal ganglia module (as in PD) leads to slow acquisition learning but intact transfer generalization. Similarly, the model shows that simulating the loss of acetylcholine in the hippocampal region (as in ACoA aneurysm) also results in slower acquisition learning. We argue from this that changes in associative learning of stimulus–action pathways (in the basal ganglia) or changes in the learning of stimulus representations (in the hippocampal region) can have similar functional effects.en_US
dc.description.sponsorshipPortions of this work were funded by the NSF/NIH Collaborative Research in Computational Neuroscience (CRCNS) Program and by NIAAA R01 AA018737 (CEM).en_US
dc.language.isoen_USen_US
dc.publisherElsevieren_US
dc.subjectHippocampal regionen_US
dc.subjectBasal gangliaen_US
dc.subjectAssociative learningen_US
dc.subjectAcquired equivalenceen_US
dc.subjectParkinson’s diseaseen_US
dc.subjectSchizophreniaen_US
dc.subjectBasal forebrainen_US
dc.subjectAmnesiaen_US
dc.subjectHippocampal atrophyen_US
dc.subjectAlzheimer’sen_US
dc.subjectDopamineen_US
dc.subjectAcetylcholineen_US
dc.titleA neural model of hippocampalstriatal interactions in associative learningand transfer generalization in various neurological and psychiatric patientsen_US
dc.typeArticleen_US


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