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Driving is a complex behavior that recruits multiple cognitive elements. We report on an imaging study of simulated driving that reveals multiple neural systems, each of which have different activation dynamics. The neural correlates of driving behavior are identified with fMRI and their modulation with speed is investigated. We decompose the activation into interpretable pieces using a novel, generally applicable approach, based upon independent component analysis. Some regions turn on or off, others exhibit a gradual decay, and yet others turn on transiently when starting or stopping driving. Signal in the anterior cingulate cortex, an area often associated with error monitoring and inhibition, decreases exponentially with a rate proportional to driving speed, whereas decreases in frontoparietal regions, implicated in vigilance, correlate with speed. Increases in cerebellar and occipital areas, presumably related to complex visuomotor integration, are activated during driving but not associated with driving speed.

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In this double-blind, placebo-controlled study, we examined the effects of subanesthetic doses of ketamine (an NMDA glutamate receptor antagonist) and thiopental (a GABA-A receptor agonist) on the event-related potential (ERP) correlates of deviant stimulus processing in 24 healthy adults. Participants completed three separate pharmacologic challenge sessions (ketamine, thiopental, saline) in a counterbalanced order. EEG data were recorded both before and during each challenge while participants performed a visual “oddball” task consisting of infrequent “target” and “novel” stimuli intermixed with frequent “standard” stimuli. We examined drug effects on the amplitude and latency of the P3(00) component of the ERP elicited by target (P3b) and novel stimuli (P3a), as well as the N2(00) and P2(00) components elicited by both targets and novels. Relative to placebo, both drugs reduced the amplitude of parietal P3b, and also tended to attenuate Target N2. Their effects on novelty processing were more differentiated. While both drugs reduced parietal P3a, this effect was greater for thiopental. Relative to placebo, ketamine also increased frontal P3a amplitude, shortened P3a latency, reduced N2, and enhanced P2 to novel stimuli.