T
Trevor W. Robbins
Researcher at University of Cambridge
Publications - 1184
Citations - 177352
Trevor W. Robbins is an academic researcher from University of Cambridge. The author has contributed to research in topics: Prefrontal cortex & Cognition. The author has an hindex of 231, co-authored 1137 publications receiving 164437 citations. Previous affiliations of Trevor W. Robbins include Centre national de la recherche scientifique & Massachusetts Institute of Technology.
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Response Disengagement on a Spatial Self-Ordered Sequencing Task: Effects of Regionally Selective Excitotoxic Lesions and Serotonin Depletion within the Prefrontal Cortex
TL;DR: The effects of selective LPFC and OFC excitotoxic lesions and 5,7-DHT-induced PFC serotonin depletions in marmosets on SSOST performance were compared and it was proposed that this deficit may be due to a failure to attend to and register that a response has been made and should not be repeated.
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Differential effects of ventral and regional dorsal striatal lesions on sucrose drinking and positive and negative contrast in rats
TL;DR: The effects of excitotoxic, fiber-sparing lesions of the ventral, medial, and lateral striatum on consummatory responses to sucrose solution rewards are compared.
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Take it or leave it: prefrontal control in recreational cocaine users
Sharon Morein-Zamir,Sharon Morein-Zamir,P. Simon Jones,Edward T. Bullmore,Trevor W. Robbins,Karen D. Ersche +5 more
TL;DR: Functional magnetic resonance imaging analyses indicated that, compared with controls, stopping in the recreational users was associated with increased activation in the pre-supplementary motor area but not the right inferior frontal cortex, which implies intact response inhibition abilities in recreational cocaine users.
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Fronto-striatal gray matter contributions to discrimination learning in Parkinson's disease.
Claire O'Callaghan,Claire O'Callaghan,Ahmed A. Moustafa,Sanne de Wit,James M. Shine,Trevor W. Robbins,Simon J.G. Lewis,Michael Hornberger +7 more
TL;DR: It is suggested that dopaminergic imbalance may not be the sole determinant of discrimination learning deficits in PD, and the importance of factoring in the broader pathological changes when constructing models of learning in PD is highlighted.