Figure 1.
Schematic illustration of a single trial.
On each trial, subjects performed a central letter identification task (a randomly rotated T or L) to ensure fixation (‘fixation task’) and identified the orientation of a peripheral target texture (horizontal or vertically aligned line segments) (‘texture discrimination task’). SOA between stimulus and mask decreased from 467 to 66 ms. Immediate auditory feedback was provided for the fixation task. Figure was adapted with permission from Schwartz et al. [43].
Figure 2.
Performance on all trials, for the fixation task and texture discrimination task (A). Performance on the texture discrimination task including only correct fixation trials (B) and including only incorrect fixation trials (C). Ketamine administration caused decreased performance on both tasks, but texture discrimination impairments were independent of fixation task performance (impairments were equal for correct and incorrect fixation trials).
Figure 3.
Performance difference between ketamine and placebo condition.
In the ketamine condition performance on the texture discrimination task is significantly more affected than performance on the fixation task, compared to the placebo condition (F(1,13) = 9.026, p = .01).
Figure 4.
Subjective state of sedation during ketamine and placebo administration.
Sedation level was based on a subset of the visual analogue scales (VAS) [41,45], filled in at different time points of the experiment. It is quantified as the distance (in mm) from a mark placed by the subject on each scale (a 100 mm line connecting two opposite states of mind), measured from the left end of the scale (see ‘Methods’ for details). Sedation levels differed between drug conditions after bolus administration (t(1,15) = -5.563, p = .00005) and at the start of the task (t(1,15) = -2.957, p = .0098). Sedation levels did not differ before drug administration (t(1,15) = .083, p = .94), but after testing subjects in the ketamine condition were still feeling slightly more sedated compared to the placebo condition (t(1,15) = -2.087, p = .054, at trend level). Within-condition, sedation levels after bolus administration and at the start of the task differed from before drug administration for the ketamine (all t(1,15)> 5.6, all p < .0005) but not for the placebo condition (within-condition p-values not depicted in this figure).
Figure 5.
Pearson’s correlation between the sedative effect of ketamine and ketamine-induced performance impairment.
The sedative effect of ketamine is measured as the sedation score, rated at the start of the task (ketamine minus placebo condition. It is quantified as the distance (in mm) from a mark placed by the subject on each scale (a 100 mm line connecting two opposite states of mind), measured from the left end of the scale (see ‘Methods’ for details). The ketamine-induced performance impairment is calculated as the average performance on the texture discrimination task (ketamine minus placebo condition). No significant correlation was observed.
Figure 6.
Reaction times on the texture discrimination task and on the fixation task were not affected during ketamine administration, indicating that ketamine-induced performance impairments were not caused by sedation (A). Ketamine administration did not slow down responses to the texture discrimination task (compared to the fixation task) any further than the placebo condition (B).