Abstract
Temporal processing of durations in the range of seconds or more is cognitively mediated, whereas processing of brief durations below 100 ms appears to be based on brain mechanisms beyond cognitive control. In a series of experiments, applying a single-behavior-multiple-brain-systems strategy, activity of various neurotransmitter systems was pharmacologically changed and effects on temporal information processing were studied. In addition, concomitant changes in different psychological functions, such as cortical arousal, speed of information processing, and memory were measured. This experimental strategy proved to be highly efficient for elucidating mechanisms underlying temporal information processing in humans. Temporal processing of durations in the range of seconds was markedly impaired by pharmacologic agents which induced deterioration of memory functions. On the other hand, temporal processing of brief durations below 100 ms was shown to be largely independent of pharmacologically induced impairment of cognitive functioning, but may rather depend on D2 receptor activity in the basal ganglia.