A Neurocomputational Model of Dopamine and Prefrontal-Striatal Interactions during Multicue Category Learning by Parkinson Patients

Autor/inn/en	Moustafa, Ahmed A.; Gluck, Mark A.
Titel	A Neurocomputational Model of Dopamine and Prefrontal-Striatal Interactions during Multicue Category Learning by Parkinson Patients
Quelle	In: Journal of Cognitive Neuroscience, 23 (2011) 1, S.151-167 (17 Seiten) PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	0898-929X
DOI	10.1162/jocn.2010.21420
Schlagwörter	Neurology; Patients; Reinforcement; Cognitive Development; Neurological Impairments; Brain Hemisphere Functions; Simulation; Biochemistry; Prediction; Task Analysis; Models; Drug Therapy; Cues + Suchen Sie Ihr Suchwort? Neurologie; Patient; Positive Verstärkung; Kognitive Entwicklung; Neurodegenerative Erkrankung; Simulation program; Simulationsprogramm; Biochemie; Vorhersage; Aufgabenanalyse; Analogiemodell; Stichwort
Abstract	Most existing models of dopamine and learning in Parkinson disease (PD) focus on simulating the role of basal ganglia dopamine in reinforcement learning. Much data argue, however, for a critical role for prefrontal cortex (PFC) dopamine in stimulus selection in attentional learning. Here, we present a new computational model that simulates performance in multicue category learning, such as the "weather prediction" task. The model addresses how PD and dopamine medications affect stimulus selection processes, which mediate reinforcement learning. In this model, PFC dopamine is key for attentional learning, whereas basal ganglia dopamine, consistent with other models, is key for reinforcement and motor learning. The model assumes that competitive dynamics among PFC neurons is the neural mechanism underlying stimulus selection with limited attentional resources, whereas competitive dynamics among striatal neurons is the neural mechanism underlying action selection. According to our model, PD is associated with decreased phasic and tonic dopamine levels in both PFC and basal ganglia. We assume that dopamine medications increase dopamine levels in both the basal ganglia and PFC, which, in turn, increase tonic dopamine levels but decrease the magnitude of phasic dopamine signaling in these brain structures. Increase of tonic dopamine levels in the simulated PFC enhances attentional shifting performance. The model provides a mechanistic account for several phenomena, including (a) medicated PD patients are more impaired at multicue probabilistic category learning than unmedicated patients and (b) medicated PD patients opt out of reversal when there are alternative and redundant cue dimensions. (As Provided).
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Update	2017/4/10