Are there dissociable roles of the mesostriatal and mesolimbocortical dopamine systems on temporal information processing in humans?
There is some experimental evidence suggesting that temporal processing of brief duration in the range of milliseconds is based on dopamine (DA)-dependent neural counting mechanisms, whereas processing of longer duration is cognitively mediated. To further elucidate the critical role of DA receptors of the D2 receptor family for temporal information processing in humans, the effects of the 3 mg of haloperidol, 300 mg of sulpiride, and 150 mg of remoxipride were studied in a placebo-controlled double-blind experiment. In addition, concomitant changes in cortical arousal as well as speed of information processing and motor execution were measured. Temporal processing of brief duration was significantly impaired by haloperidol (p < 0.01) but not by sulpiride and remoxipride, whereas processing of longer duration was adversely affected by haloperidol (p < 0.001) as well as remoxipride (p < 0.01) as compared to placebo. The pattern of results in combination with the different pharmacological profiles of the dopaminergic drugs applied in the present study suggests that temporal processing of brief duration is mediated by D2 receptor activity in the mesostriatal system and, thus, point to the basal ganglia as a neuroanatomical structure possibly involved in timing of brief duration. On the other hand, deteriorating effects of D2 receptor blockers on processing of longer duration appear to be due to DA-induced impairment of memory functions which may be mediated by the mesolimbocortical DA system.
Rammsayer
T H
TH
Institute of Psychology, University of Jena, Germany.
D000328:Adult; D001143:Arousal / Q000187:drug effects / Q000502:physiology; D001288:Attention / Q000187:drug effects / Q000502:physiology*; D001479:Basal Ganglia / Q000187:drug effects / Q000502:physiology; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D003342:Corpus Striatum / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000502:physiology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D005425:Flicker Fusion / Q000187:drug effects / Q000502:physiology; D006220:Haloperidol / Q000494:pharmacology; D006801:Humans; D008032:Limbic System / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008636:Mesencephalon / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000502:physiology; D017330:Remoxipride / Q000494:pharmacology; D012684:Sensory Thresholds / Q000187:drug effects / Q000502:physiology; D013469:Sulpiride / Q000494:pharmacology; D013998:Time Perception / Q000187:drug effects / Q000502:physiology*
D018492:Dopamine Antagonists; D017448:Receptors, Dopamine D2; D017330:Remoxipride; D013469:Sulpiride; D006220:Haloperidol; D004298:Dopamine