Original Research ARTICLE
The effect of moderate acute psychological stress on working memory-related neural activity is modulated by a genetic variation in catecholaminergic function in humans
- 1Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands
- 2Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA
- 3Department of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK
- 4Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China
- 5Beijing Key Laboratory of Learning and Cognition, Department of Psychology, Capital Normal University, Beijing, China
- 6Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands
- 7Department for Cognitive Neuroscience, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands
Acute stress has an important impact on higher-order cognitive functions supported by the prefrontal cortex (PFC) such as working memory (WM). In rodents, such effects are mediated by stress-induced alterations in catecholaminergic signaling, but human data in support of this notion is lacking. A common variation in the gene encoding Catechol-O-methyltransferase (COMT) is known to affect basal catecholaminergic availability and PFC functions. Here, we investigated whether this genetic variation (Val158Met) modulates effects of stress on WM-related neural activity in humans. In a counterbalanced crossover design, 41 healthy young men underwent functional magnetic resonance imaging (fMRI) while performing a numerical N-back WM task embedded in a stressful or neutral context. Moderate psychological stress was induced by a well-controlled procedure involving viewing strongly aversive (versus emotionally neutral) movie material in combination with a self-referencing instruction. Acute stress resulted in genotype-dependent effects on WM performance and WM-related activation in the dorsolateral PFC, with a relatively negative impact of stress in COMT Met-homozygotes as opposed to a relatively positive effect in Val-carriers. A parallel interaction was found for WM-related deactivation in the anterior medial temporal lobe (MTL). Our findings suggest that individuals with higher baseline catecholaminergic availability (COMT Met-homozygotes) appear to reach a supraoptimal state under moderate levels of stress. In contrast, individuals with lower baselines (Val-carriers) may reach an optimal state. Thus, our data show that effects of acute stress on higher-order cognitive functions vary depending on catecholaminergic availability at baseline, and thereby corroborate animal models of catecholaminergic signaling that propose a non-linear relationship between catecholaminergic activity and prefrontal functions.
Keywords: stress, working memory, Catechol-O-methyltransferase, catecholamine, prefrontal cortex, fMRI
Citation: Qin S, Cousijn H, Rijpkema M, Luo J, Franke B, Hermans EJ and Fernández G (2012) The effect of moderate acute psychological stress on working memory-related neural activity is modulated by a genetic variation in catecholaminergic function in humans. Front. Integr. Neurosci. 6:16. doi: 10.3389/fnint.2012.00016
Received: 30 November 2011; Accepted: 07 April 2012;
Published online: 11 May 2012.
Edited by:Florin Dolcos, University of Illinois Urbana-Champaign, USA
Reviewed by:Barry Setlow, University of Florida, USA
Antonio Pereira, Federal University of Rio Grande do Norte, Brazil
Nicole Oei, Leiden University Medical Center, Netherlands
Copyright: © 2012 Qin, Cousijn, Rijpkema, Luo, Franke, Hermans and Fernández. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits noncommercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
*Correspondence: Shaozheng Qin, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA 94305-5719, USA. e-mail: email@example.com