The Effects of Acute Dopamine Precursor Depletion on the Cognitive Control Functions of Performance Monitoring and Conflict Processing: An Event-Related Potential (ERP) Study.
Studies using medications and psychiatric populations implicate dopamine in cognitive control and performance monitoring processes. However, side effects associated with medication or studying psychiatric groups may confound the relationship between dopamine and cognitive control. To circumvent such possibilities, we utilized a randomized, double-blind, placebo-controlled, within-subjects design wherein participants were administered a nutritionally-balanced amino acid mixture (BAL) and an amino acid mixture deficient in the dopamine precursors tyrosine (TYR) and phenylalanine (PHE) on two separate occasions. Order of sessions was randomly assigned. Cognitive control and performance monitoring were assessed using response times (RT), error rates, the N450, an event-related potential (ERP) index of conflict monitoring, the conflict slow potential (conflict SP), an ERP index of conflict resolution, and the error-related negativity (ERN) and error positivity (Pe), ERPs associated with performance monitoring. Participants were twelve males who completed a Stroop color-word task while ERPs were collected four hours following acute PHE and TYR depletion (APTD) or balanced (BAL) mixture ingestion in two separate sessions. N450 and conflict SP ERP amplitudes significantly differentiated congruent from incongruent trials, but did not differ as a function of APTD or BAL mixture ingestion. Similarly, ERN and Pe amplitudes showed significant differences between error and correct trials that were not different between APTD and BAL conditions. Findings indicate that acute dopamine precursor depletion does not significantly alter cognitive control and performance monitoring ERPs. Current results do not preclude the role of dopamine in these processes, but suggest that multiple methods for dopamine-related hypothesis testing are needed.
Department of Psychology, Brigham Young University, Provo, Utah, United States of America, 84602; Neuroscience Center, Brigham Young University, Provo, Utah, United States of America, 84602.
Michael J
MJ
Larson
Department of Psychology, Brigham Young University, Provo, Utah, United States of America, 84602; Department of Psychology, University of California Los Angeles, Los Angeles, California, United States of America, 90095.
Peter E
PE
Clayson
Department of Psychology, Brigham Young University, Provo, Utah, United States of America, 84602.
Mark
M
Primosch
Department of Psychiatry, McGill University, 1033 Pine Ave. W., Montreal, QC, Canada, H3A 1A1.
Marco
M
Leyton
Department of Psychology, Brigham Young University, Provo, Utah, United States of America, 84602; Neuroscience Center, Brigham Young University, Provo, Utah, United States of America, 84602.
Scott C
SC
Steffensen
D003071:Cognition / Q000502:physiology; D004298:Dopamine / Q000378:metabolism*; D004311:Double-Blind Method; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D009483:Neuropsychological Tests; D010649:Phenylalanine / Q000172:deficiency; D011597:Psychomotor Performance; D011930:Reaction Time / Q000502:physiology; D014443:Tyrosine / Q000172:deficiency
D014443:Tyrosine; D010649:Phenylalanine; D004298:Dopamine