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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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Noradrenergic versus dopaminergic modulation of impulsivity, attention and monitoring behaviour in rats performing the stop-signal task

TL;DR: The results suggest that the use of specific pharmacological agents targeting α2 and β noradrenergic receptors may improve existing treatments for attentional deficits and impulsivity, whereas DA D3 receptors may modulate error monitoring and perseverative behaviour.
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Effects of excitotoxic lesions of the central amygdaloid nucleus on the potentiation of reward-related stimuli by intra-accumbens amphetamine.

TL;DR: Lesions of the central nucleus of the amygdala did not impair the performance of positively reinforced discriminated approach, nor did they impair the acquisition of a new response with conditioned reinforcement, however, the potentiation of responding with CR following intra-accumbens amphetamine was blocked in lesioned animals.
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Enduring Deficits in Sustained Visual Attention during Withdrawal of Intravenous Methylenedioxymethamphetamine Self-Administration in Rats: Results from a Comparative Study with d -Amphetamine and Methamphetamine

TL;DR: The findings show that amphetamine-derived stimulants have both short- and long-term consequences for psychomotor functioning, and the demonstration of residual deficits in rats chronically exposed to MDMA raises some concern about the potential harm caused by this drug in human ecstasy users.
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Apathy and impulsivity in frontotemporal lobar degeneration syndromes

TL;DR: In this article, the NIHR Cambridge Biomedical Research Centre with additional support from the Cambridge Home and EU Scholarship Scheme, the James F McDonnell Foundation (21st Century Science Initiative for Understanding Human Cognition), Wellcome Trust (103838); Medical Research Council (MC US A060 0016, and RG62761), the Cambridge Brain Bank, PSP Association and the Evelyn Trust.
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Task-Set Switching Deficits in Early-Stage Huntington's Disease: Implications for Basal Ganglia Function

TL;DR: Alterations in the "response-setting" process alone and both the response-setting and "response inhibition" process probably arise from striatal pathology in HD, thus accounting for the task-switching deficits and showing how basal ganglia implemented response processes may underpin executive function.