98%
921
2 minutes
20
The constant interplay between affective processing and cognitive control supports emotion regulation and appropriate social functioning. Even when affective stimuli are processed implicitly, threat-related stimuli are prioritized in the earliest stages of processing; yet, it remains unclear how implicit attention to affect influences subsequent cognitive control functions. The present study evaluated the influence of affective valence on early perceptual processes and subsequent response inhibition in a context where affective properties of the stimuli (facial expressions) were not critical for performing the task. Participants (N = 32) completed an affective stop-signal task (SST) while their scalp EEGs were recorded. The SST assessed response inhibition while participants implicitly attended to happy and afraid facial expressions that were matched for level of arousal. Behavioral performance was measured via response time and accuracy while physiological response was measured via the P100, N170, and N200/P300 ERP components. Decreased gender discrimination accuracy, delayed P100 latency, and more negative N170 amplitude were observed for afraid faces compared to happy faces, suggesting a shift in processing with respect to face valence. However, differences in stopping accuracy or N200/P300 ERP components during response inhibition were not observed, pointing to top-down cognitive processes likely being recruited to override the early automatic response to prioritize threat-related stimuli. Findings highlight that, in this implicit affective attention task, threat-related stimuli are prioritized early during processing, but implicitly attending to differentially valenced stimuli did not modulate subsequent cognitive control functions.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/psyp.13467 | DOI Listing |
Plant Cell
September 2025
Department of Plant Sciences, College of Biological Sciences, State Key Laboratory of Plant Environmental Resilience, China Agricultural University, Beijing 100193, China.
Plant thermomorphogenesis is a critical adaptive response to elevated ambient temperatures. The transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) integrates diverse environmental and phytohormone signals to coordinate thermoresponsive growth. However, the cellular mechanisms underlying plant thermomorphogenic growth remain poorly understood.
View Article and Find Full Text PDFSci Signal
September 2025
Department of Surgery, University of Alabama Birmingham, Birmingham, AL 35233, USA.
Amphetamines are psychostimulants that are commonly used to treat neuropsychiatric disorders and are prone to misuse. The pathogenesis of amphetamine use disorder (AUD) is associated with dysbiosis (an imbalance in the body's microbiome) and bacterially produced short-chain fatty acids (SCFAs), which are implicated in the gut-brain axis. Amphetamine exposure in both rats and humans increases the amount of intestinal , which releases SFCAs.
View Article and Find Full Text PDFElife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
View Article and Find Full Text PDFJ Neurophysiol
September 2025
Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Schubertstrasse 42, 01307 Dresden, Germany.
Cognitive control - the ability to regulate information processing in line with current goals - is essential for cognitive functioning. We examined whether uncertainty in cognitive control demands leads to higher processing of cues that reduce uncertainty. Participants completed a Go/NoGo task with two NoGo:Go ratios (4:5 and 1:6).
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
Department of Medical Biology, Faculty of Medicine, Bahçeşehir University, Istanbul 34353, Turkey.
IL-17A is a pro-inflammatory cytokine that significantly contributes to the pathogenesis of autoimmune diseases, including multiple sclerosis (MS). Previous studies have suggested that PARP-1 inhibitors can modulate IL-17A-mediated inflammation, prompting the investigation of Niraparib, an FDA-approved PARP-1 inhibitor, as a potential therapeutic agent for MS. In this study, we hypothesized that Niraparib could disrupt the interaction between IL-17A and its receptor, IL-17RA.
View Article and Find Full Text PDF