Contribution of the primate prefrontal cortex to the gap effect.

The introduction of a brief temporal gap between the disappearance of the initial fixation point and the presentation of a peripheral target leads to a general reduction in saccadic reaction times (SRTs), known as the gap effect. Moreover, extremely short latency express saccades frequently occur in this paradigm. Disorders of the prefrontal cortex (PFC) are often associated with increased numbers of express saccades and an inability to suppress reflexive saccades. To investigate the role of the PFC in the gap effect and in express saccade generation, we trained two rhesus monkeys on a gap saccade task in which the initial fixation point (FP) disappeared 200 ms or 600 ms before a peripheral stimulus appeared either 8 degrees to its left or right side. We recorded from the lateral PFC (areas 8 Ar and 46) in both monkeys the activity of 214 neurons, 84 (39%) of which exhibited task-related activity. These neurons could be further categorized into separate groups based on their discharge behaviour: fixation neurons with a decrease in activity during the gap (27%), FP offset neurons (12%), preparatory neurons with an increase in activity during the gap (30%), visual neurons (6%), post-saccadic neurons (8%), and reward-related neurons (12%). There were no obvious differences in the topography of these groups. Significant differences between express and regular saccade trials were found for fixation-related neurons. These neurons had a lower activity during the gap prior to the generation of contralateral express saccades. We hypothesize that a reduction in the activity of fixation-related neurons in the PFC may contribute to the elevated rate of express saccades in prefrontal disorders.