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The Journal of Neuroscience, November 26, 2008, 28(48):12868-12876; doi:10.1523/JNEUROSCI.3592-08.2008
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Behavioral/Systems/Cognitive
Modeling a Negative Response Bias in the Human Amygdala by Noradrenergic–Glucocorticoid Interactions
Juraj Kukolja,1,2,4 Thomas E. Schläpfer,2 Christian Keysers,5 Dietrich Klingmüller,3 Wolfgang Maier,2 Gereon R. Fink,1,4 andRené Hurlemann2 1Cognitive Neurology Section, Institute of Neuroscience and Biophysics–Medicine, Research Centre Juelich, 52425 Juelich, Germany, Departments of 2Psychiatry, and 3Clinical Biochemistry, Division of Endocrinology, University of Bonn, 53105 Bonn, Germany, 4Department of Neurology, University Hospital, Cologne University, 50924 Cologne, Germany, and 5Behavioral and Cognitive Neuroscience NeuroImaging Center, University Medical Center Groningen, 9713 AW Groningen, The Netherlands
Correspondence should be addressed to either of the following: Dr. Juraj Kukolja, Department of Neurology, University Hospital, Cologne University, Kerpener Strasse 62, 50924 Cologne, Germany, Email: juraj.kukolja{at}uk-koeln.de; or Dr. René Hurlemann, Department of Psychiatry, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany, E-mail: Email: renehurlemann{at}me.com
An emerging theme in the neuroscience of emotion is the question of how acute stress shapes, and distorts, social-emotional behavior. The prevailing neurocircuitry models of social-emotional behavior emphasize the central role of the amygdala. Acute stress leads to increased central levels of norepinephrine (NE) and cortisol (CORT), and evidence suggests that these endogenous neuromodulators synergistically influence amygdala responses to social-emotional stimuli. We therefore hypothesized that amygdala responses to emotional facial expressions would be susceptible to pharmacologically induced increases in central NE and CORT levels. To specifically test this hypothesis, we measured amygdala activation to emotional faces using functional magnetic resonance imaging in 62 healthy subjects under four pharmacological conditions: (1) single oral dose of placebo, (2) 4 mg of the selective NE-reuptake inhibitor reboxetine (RBX), (3) 30 mg of hydrocortisone, or (4) both drugs in combination. We found that a decrease in amygdala activation to positive facial emotion was coupled with an increase in amygdala activation to negative facial emotion in the RBX-CORT combined challenge condition. In conclusion, a pharmacologically induced elevation of central NE and CORT levels in healthy subjects created a negative response bias in the amygdala that did not exist at baseline. Our results implicate a causative role of NE–CORT interactions in the emergence of a negative bias of cognitive and emotional functions which is germane in stress-related affective spectrum disorders.
Key words: norepinephrine; cortisol; amygdala; emotion; stress; major depressive illness
Received July 30, 2008; revised Oct. 14, 2008; accepted Oct. 14, 2008.
Correspondence should be addressed to either of the following: Dr. Juraj Kukolja, Department of Neurology, University Hospital, Cologne University, Kerpener Strasse 62, 50924 Cologne, Germany, Email: juraj.kukolja{at}uk-koeln.de; or Dr. René Hurlemann, Department of Psychiatry, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany, E-mail: Email: renehurlemann{at}me.com
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[Abstract] [Full Text] [PDF]
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