T
Thomas A. Stalnaker
Researcher at National Institute on Drug Abuse
Publications - 41
Citations - 3818
Thomas A. Stalnaker is an academic researcher from National Institute on Drug Abuse. The author has contributed to research in topics: Orbitofrontal cortex & Associative learning. The author has an hindex of 25, co-authored 39 publications receiving 3433 citations. Previous affiliations of Thomas A. Stalnaker include University of Maryland, Baltimore & National Institutes of Health.
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A new perspective on the role of the orbitofrontal cortex in adaptive behaviour
TL;DR: It is suggested that the function of the orbitofrontal cortex is crucial for signalling outcome expectancies and can also explain the crucial role of the OFC in changing behaviour in the face of unexpected outcomes.
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Orbitofrontal cortex, decision-making and drug addiction
TL;DR: This review will discuss recent evidence that supports this proposal and examine evidence that loss of this signal, as the result of drug-induced changes in these brain circuits, might account for the maladaptive decision-making that characterizes drug addiction.
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What the orbitofrontal cortex does not do
TL;DR: The proposed roles for OFC are considered, critically examining the level of support for these claims and highlighting the data that call them into question.
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The orbitofrontal cortex and ventral tegmental area are necessary for learning from unexpected outcomes
Yuji K. Takahashi,Matthew R. Roesch,Thomas A. Stalnaker,Richard Z. Haney,Donna J. Calu,Adam R. Taylor,Kathryn A. Burke,Geoffrey Schoenbaum,Geoffrey Schoenbaum +8 more
TL;DR: It is shown that signaling of reward predictions by OFC neurons was related to signaling of prediction errors by dopamine neurons in ventral tegmental area (VTA), and bilateral inactivation of VTA or contralateral in activation of Vta and OFC disrupted learning driven by unexpected outcomes.
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Basolateral Amygdala Lesions Abolish Orbitofrontal-Dependent Reversal Impairments
TL;DR: A critical test of the hypothesis that the reversal deficit in OFC-lesioned rats is caused by this inflexible encoding in ABL, and results are consistent with the hypotheses that OFC facilitates cognitive flexibility by promoting updating of associative encoding in downstream brain areas.