Acute serotonin and dopamine depletion improves attentional control: findings from the stroop task.
Schizophrenia is associated with impairments of attentional control on classic experimental paradigms such as the Stroop task. However, at a basic level the neurochemical mechanisms that may be responsible for such impairments are poorly understood. In this study, we sought to investigate the influence of brain monoamine function on Stroop task performance in healthy participants using the established methods of acute dietary serotonin, dopamine, and combined monoamine depletion. The study was a double-blind placebo controlled design in which 12 healthy male participants completed the Stroop task under four acute treatment conditions: (a) balanced/placebo control, (b) acute tryptophan depletion, (c) acute tyrosine/phenylalanine depletion, and (d) acute tyrosine/phenylalanine/tryptophan depletion (combined monoamine depletion). Decreased Stroop interference indicating improved attentional control was observed after both tryptophan depletion and tyrosine/phenylalanine depletion, while there was no significant change in interference after combined monoamine depletion. Findings suggest that reduced tonic dopamine or serotonin activity within specific neural circuits (such as the striatum, anterior cingulate, or prefrontal cortex) may play a critical role in attentional control, possibly by improving gating of information via reducing noise in monoaminergic systems. These findings enhance our understanding of the neurochemical basis of attentional control and the possible cause of attentional control deficits in schizophrenia.
Scholes
Kirsty E
KE
Behavioural Neuroscience Laboratory, Department of Physiology, Monash Centre for Brain and Behavior, Monash University, Melbourne, VIC, Australia.
Harrison
Ben J
BJ
O'Neill
Barry V
BV
Leung
Sumie
S
Croft
Rodney J
RJ
Pipingas
Andrew
A
Phan
K Luan
KL
Nathan
Pradeep J
PJ
D000328:Adult; D001288:Attention / Q000187:drug effects / Q000502:physiology*; D015306:Biogenic Monoamines / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000378:metabolism*; D004311:Double-Blind Method; D006801:Humans; D008297:Male; D019964:Mood Disorders / Q000378:metabolism / Q000503:physiopathology; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism; D009483:Neuropsychological Tests; D010919:Placebos; D012559:Schizophrenia / Q000378:metabolism* / Q000503:physiopathology; D012701:Serotonin / Q000172:deficiency* / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014364:Tryptophan / Q000172:deficiency; D014443:Tyrosine / Q000172:deficiency
D015306:Biogenic Monoamines; D010919:Placebos; D012701:Serotonin; D014443:Tyrosine; D014364:Tryptophan; D004298:Dopamine