Cognitive regulation of saccadic velocity by reward prospect

It is known that expectation of reward speeds up saccades. Past studies have also shown the presence of a saccadic velocity bias in the orbit, resulting from a biomechanical regulation over varying eccentricities. Nevertheless, whether and how reward expectation interacts with the biomechanical regulation of saccadic velocities over varying eccentricities remains unknown. We addressed this question by conducting a visually guided double‐step saccade task. The role of reward expectation was tested in monkeys performing two consecutive horizontal saccades, one associated with reward prospect and the other not. To adequately assess saccadic velocity and avoid adaptation, we systematically varied initial eye positions, saccadic directions and amplitudes. Our results confirmed the existence of a velocity bias in the orbit, i.e., saccadic peak velocity decreased linearly as the initial eye position deviated in the direction of the saccade. The slope of this bias increased as saccadic amplitudes increased. Nevertheless, reward prospect facilitated velocity to a greater extent for saccades away from than for saccades toward the orbital centre, rendering an overall reduction in the velocity bias. The rate (slope) and magnitude (intercept) of reward modulation over this velocity bias were linearly correlated with amplitudes, similar to the amplitude‐modulated velocity bias without reward prospect, which presumably resulted from a biomechanical regulation. Small‐amplitude (≤ 5°) saccades received little modulation. These findings together suggest that reward expectation modulated saccadic velocity not as an additive signal but as a facilitating mechanism that interacted with the biomechanical regulation. This study showed that, without reward prospect, saccadic peak velocity decreased linearly as initial eye position deviated in the direction of the saccade. However, with reward prospect, the slope (rate) and the intercept (magnitude) of the velocity bias was reduced and increased, respectively, with amplitude. The findings suggest that reward modulation was not an additive signal, but as a facilitating mechanism that interacted with the biomechanical regulation.