Reward and cognitive control play crucial roles in shaping goal-directed behavior. Yet, the behavioral and neural underpinnings of interactive effects of both processes in driving our actions towards a particular goal have remained rather unclear. Given the importance of inhibitory control, we investigated the effect of reward prospect on the modulatory influence of automatic versus controlled processes during response inhibition. For this, a performance-contingent monetary reward for both correct response selection and response inhibition was added to a Simon NoGo task, which manipulates the relationship of automatic and controlled processes in Go and NoGo trials. A neurophysiological approach was used by combining EEG temporal signal decomposition and source localization methods. Compared to a non-rewarded control group, rewarded participants showed faster response execution, as well as overall lower response selection and inhibition accuracy (shifted speed-accuracy tradeoff). Interestingly, the reward group displayed a larger interference of the interactive effects of automatic versus controlled processes during response inhibition (i.e., a larger Simon NoGo effect), but not during response selection. The reward-specific behavioral effect was mirrored by the P3 amplitude, underlining the importance of stimulus-response association processes in explaining variability in response inhibition performance. The selective reward-induced neurophysiological modulation was associated with lower activation differences in relevant structures spanning the inferior frontal and parietal cortex, as well as higher activation differences in the somatosensory cortex. Taken together, this study highlights relevant neuroanatomical structures underlying selective reward effects on response inhibition and extends previous reports on the possible detrimental effect of reward-triggered performance trade-offs on cognitive control processes.
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http://dx.doi.org/10.1038/s41598-023-37524-z | DOI Listing |
Chem Res Toxicol
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Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, 4770 Buford Highway NE, Atlanta, Georgia 30341, United States.
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View Article and Find Full Text PDFAppl Biochem Biotechnol
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Department of Internal Medicine-Cardiovascular, Guangzhou Twelfth People's Hospital, No.1, Tianqiang Road, Tianhe District, Guangzhou City, Guangdong Province, 510620, China.
Myocardial infarction (MI) is a coronary artery-related disease that seriously threatens human life and is the leading cause of sudden death worldwide, where a lack of nutrients and oxygen leads to an inflammatory response and death of cardiomyocytes. Ferroptosis is a form of non-apoptotic cell death associated with metabolic dysfunction, resulting in abnormal breakdown of glutamine and iron-dependent accumulation of reactive oxygen species (ROS) during metabolism. However, the molecular mechanism of ferroptosis in the pathogenesis of MI and the function of Klotho and KRAS on ferroptosis during MI remain unclear.
View Article and Find Full Text PDFMetab Brain Dis
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Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
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View Article and Find Full Text PDFPsychopharmacology (Berl)
January 2025
Department of Molecular Biology, Ariel University, Ariel, Israel.
Rationale: Rapid adaptation to stressful events is essential for survival and requires acute stress response and stress-coping strategy. However, the molecular mechanisms that govern this coping strategy have yet to be fully discovered.
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Sci China Life Sci
January 2025
Institute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center; Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, 100191, China.
Diffuse-type tenosynovial giant cell tumor (dTGCT) is a destructive but rare benign proliferative synovial neoplasm. Although surgery is currently the main treatment modality for dTGCT, the recurrence risk is up to 50%. Therefore, there is a great need for effective drugs against dTGCT with minor side effects.
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