Beta receptor-mediated modulation of the oddball P3 but not error-related ERP components in humans

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• 作者：Mischa de Rover ; Stephen B. R. E. Brown ; Guido P. Band…
• 关键词：Beta ; blockers ; Norepinephrine ; P300 ; ERP ; EEG ; Error processing ; Post ; error slowing ; Conflict adaptation ; Antagonist ; Inverted U
• 刊名：Psychopharmacology
• 出版年：2015
• 出版时间：September 2015
• 年：2015
• 卷：232
• 期：17
• 页码：3161-3172
• 全文大小：1,043 KB
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• 作者单位：Mischa de Rover (1) (2)
  Stephen B. R. E. Brown (2) (3)
  Guido P. Band (2) (3)
  Erik J. Giltay (4)
  Martijn S. van Noorden (4)
  Nic J. A. van der Wee (2) (4)
  Sander Nieuwenhuis (2) (3)
  
  1. Clinical Psychology Unit, Institute of Psychology, Leiden University, Wassenaarseweg 52, 2333 AK, Leiden, The Netherlands
  2. Leiden Institute for Brain and Cognition (LIBC), Leiden University, Leiden, The Netherlands
  3. Cognitive Psychology Unit, Institute of Psychology, Leiden University, Leiden, The Netherlands
  4. Department of Psychiatry, Leiden University Medical Center, Leiden, The Netherlands
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Pharmacology and Toxicology
  Psychiatry
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-2072

文摘

Rationale The P3 is a ubiquitous component of stimulus-driven neural activity that can be observed in scalp electrophysiological recordings. Multiple lines of evidence suggest an important role for the noradrenergic system in the generation of the P3. However, pharmacological studies of the P3 using noradrenergic manipulations have so far been limited to agents that affect α2-receptor signaling. Objectives The present study investigated whether β-adrenergic receptors are involved in the generation of the P3 and the error positivity (Pe), a component of the event-related potential that is elicited by errors and that bears many similarities to the P3. Methods We used a double-blind, placebo-controlled, crossover design in which we examined in human participants (N--6) the effect of a single dose of propranolol (80?mg) on the amplitudes of the P3 observed in visual and auditory oddball tasks and the Pe observed in a flanker task. Results We found that P3s to auditory stimuli were increased in amplitude following treatment with propranolol. Propranolol also modulated the P3 to visual stimuli, but in a direction dependent on participants-level of trait anxiety: In participants with lower trait anxiety, propranolol resulted in a (non-significant) decrease in P3 amplitudes; in participants with higher trait anxiety, propranolol significantly enhanced P3 amplitude. Propranolol did not modulate the amplitude of the Pe or behavioral measures of conflict/error-related performance adjustments. Conclusions These results provide the first evidence for involvement of β-adrenergic receptors in P3 generation. We speculate that propranolol affected the P3 through actions at β2-receptors in the locus coeruleus.