J
Jeremy K. Seamans
Researcher at University of British Columbia
Publications - 78
Citations - 12099
Jeremy K. Seamans is an academic researcher from University of British Columbia. The author has contributed to research in topics: Prefrontal cortex & Working memory. The author has an hindex of 45, co-authored 76 publications receiving 11311 citations. Previous affiliations of Jeremy K. Seamans include Medical University of South Carolina & Salk Institute for Biological Studies.
Papers
More filters
Journal ArticleDOI
The principal features and mechanisms of dopamine modulation in the prefrontal cortex
TL;DR: Certain principles of DA mechanisms are identified by drawing on published, as well as unpublished data from PFC and other CNS sites to shed light on aspects of DA neuromodulation and address some of the existing controversies.
Journal ArticleDOI
Dopamine receptor signaling.
TL;DR: The D1-like and D2-like classes of dopamine receptors each has shared signaling properties that contribute to the definition of the receptor class, although some differences among subtypes within a class have been identified.
Journal ArticleDOI
Selective Roles for Hippocampal, Prefrontal Cortical, and Ventral Striatal Circuits in Radial-Arm Maze Tasks With or Without a Delay
TL;DR: Functional interactions between the hippocampus, the prefrontal cortex, and the ventral striatum in rats during the performance of delayed and nondelayed spatially cued radial-arm maze tasks suggest that different aspects of spatially mediated behavior are subserved by separate, distributed limbic–cortical–striatal networks.
Journal ArticleDOI
Neurocomputational models of working memory.
TL;DR: The models show how sustained activity can be stable in the presence of noise and distractors, how different synaptic and voltage-gated conductances contribute to persistent activity, how neuromodulation could influence its robustness, how completely novel items could be maintained, and how continuous attractor states might be achieved.
Journal ArticleDOI
Unmanageable motivation in addiction: a pathology in prefrontal-accumbens glutamate transmission.
TL;DR: A hypothesis is articulated that altered G protein signaling in the PFC focuses behavior on drug-associated stimuli, while dysregulated PFC-accumbens synaptic glutamate transmission underlies the unmanageable motivation to seek drugs.