Background: Acute psychological stress impairs higher-order cognitive function such as working memory (WM). Similar impairments are seen in various psychiatric disorders that are associated with higher susceptibility to stress and with prefrontal cortical dysfunctions, suggesting that acute stress may play a potential role in such dysfunctions. However, it remains unknown whether acute stress has immediate effects on WM-related prefrontal activity.
Methods: Using functional magnetic resonance imaging (fMRI), we investigated neural activity of 27 healthy female participants during a blocked WM task (numerical N-back) while moderate psychological stress was induced by viewing strongly aversive (vs. neutral) movie material together with a self-referencing instruction. To assess stress manipulation, autonomic and endocrine, as well as subjective, measurements were acquired throughout the experiment.
Results: Successfully induced acute stress resulted in significantly reduced WM-related activity in the dorsolateral prefrontal cortex (DLPFC), and was accompanied by less deactivation in brain regions that are jointly referred to as the default mode network.
Conclusions: This study demonstrates that experimentally induced acute stress in healthy volunteers results in a reduction of WM-related DLPFC activity and reallocation of neural resources away from executive function networks. These effects may be explained by supraoptimal levels of catecholamines potentially in conjunction with elevated levels of cortisol. A similar mechanism involving acute stress as a mediating factor may play an important role in higher-order cognitive deficits and hypofrontality observed in various psychiatric disorders.
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http://dx.doi.org/10.1016/j.biopsych.2009.03.006 | DOI Listing |
Tissue Cell
January 2025
Department of Human and Animal Physiology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia; Research Institute of Biology, Yerevan State University, Yerevan, 1 Alek Manukyan St, Yerevan 0025, Armenia. Electronic address:
High altitude characterized by the low partial pressure of the oxygen is a life-threatening condition that contributes to the development of acute pulmonary edema and hypoxic lung injury. In this study, we aimed to investigate the contribution of some inflammatory and oxidative stress markers along with antioxidant system enzymes in the pathogenesis of HAPE (high-altitude pulmonary edema) formation. We incorporated the study on 42 male rats to unravel the role of mast cells (MCs) and TNF-α in the lung after the effect of acute hypobaric hypoxia.
View Article and Find Full Text PDFJ Trauma Acute Care Surg
November 2024
From the Department of Surgery and Sepsis and Critical Illness Research Center (J.A.M., L.S.K., E.E.P., C.G.A., K.B.K., L.E.B., P.A.E., A.M.M.), University of Florida College of Medicine, Gainesville; and The Gut Biome Lab, Department of Health, Nutrition, and Food Sciences (G.P., R.N.), Florida State University College of Education, Health, and Human Sciences, Tallahassee, Florida.
Background: Traumatic injury leads to gut dysbiosis with changes in microbiome diversity and conversion toward a "pathobiome" signature characterized by a selective overabundance of pathogenic bacteria. The use of non-selective beta antagonism in trauma patients has been established as a useful adjunct to reduce systemic inflammation. We sought to investigate whether beta-adrenergic blockade following trauma would prevent the conversion of microbiome to a "pathobiome" phenotype.
View Article and Find Full Text PDFIntensive Care Med Exp
January 2025
Intensive Care Unit, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, 530021, Guangxi, China.
Background: Sepsis-induced acute lung injury (S-ALI) significantly contributes to unfavorable clinical outcomes. Emerging evidence suggests a novel role for ferroptosis in the pathophysiology of ALI, though the precise mechanisms remain unclear. Mild hypothermia (32-34 °C) has been shown to inhibit inflammatory responses, reduce oxidative stress, and regulate metabolic processes.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Faculty of Applied Sciences & Biotechnology, Shoolini University, Solan, 173229, India.
Background: The role and relevance of macrophages both as causes and therapeutics of cellular senescence is rapidly emerging. However, current knowledge regarding the extent and depth of senescence in macrophages in vivo is limited and controversial. Further, acute models of stress-induced senescence in transformed/cancerous macrophage cell lines are being used although their efficacy and relevance are not characterized.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Weatherhead P.E.T. Imaging Center, McGovern Medical School at UTHealth, Houston, Texas, USA.
An increasing number of procedures over the past two decades for aortic stenosis (AS) reflects the combination of an aging population and less invasive transcatheter options. As a result, the hemodynamics of the aortic valve (AV) have gained renewed interest to understand its behavior and to optimize patient selection. We studied the hemodynamic relationship between pressure loss (ΔP) and transvalvular flow (Q) of the normal AV as well as the impact of a variable supravalvular stenosis.
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