Journal
BEHAVIORAL NEUROSCIENCE
Volume 120, Issue 3, Pages 497-517Publisher
AMER PSYCHOLOGICAL ASSOC
DOI: 10.1037/0735-7044.120.3.497
Keywords
basal ganglia; dopamine; cognition; computational; psychopharmacology
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Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000051] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH069597] Funding Source: NIH RePORTER
- NCRR NIH HHS [M01RR00051] Funding Source: Medline
- NIMH NIH HHS [MH069597-01] Funding Source: Medline
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The authors test a neurocomputational model of dopamine function in cognition by administering to healthy participants low doses of D-2 agents cabergoline and haloperidol. The model suggests that DA dynamically modulates the balance of Go and No-Go basal ganglia pathways during cognitive learning and performance. Cabergoline impaired, while haloperidol enhanced, Go learning from positive reinforcement, consistent with presynaptic drug effects. Cabergoline also caused an overall bias toward Go responding, consistent with postsynaptic action. These same effects extended to working memory and attentional domains, supporting the idea that the basal ganglia/dopamine system modulates the updating of prefrontal representations. Drug effects interacted with baseline working memory span in all tasks. Taken together, the results support a unified account of the role of dopamine in modulating cognitive processes that depend on the basal ganglia.
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