Figure 1. Conceptual schematic of saccade and pre-saccade motor potential revealed by disinhibition.

(a) Under normal conditions, premotor activity accumulates at different rates on different trials (three example traces in top row) to a movement initiation criterion, opening downstream gating (thick red line) and triggering the saccade following an efferent delay (~20 ms, green window). Following saccade onset, variation in neural activity is correlated with variation in saccade velocity (match gray scale in top and bottom rows), indicating the neuron’s motor potential. (b) Removal of inhibition through an experimental manipulation at an earlier time (thick red line), during saccade preparation and before the typical movement criterion is reached. The disinhibition may reveal the motor potential of ongoing activity in the form of correlated kinematics of the eye before onset of the actual saccade (light red region, velocity traces in bottom row), and also allows us to study any changes in the dynamics of activity leading up to the reduced latency saccades (dashed activity traces in top row). (c) Schematic of the premotor circuitry involved in saccade generation. A desired displacement command (or, as tested here, a kinematics-driving command) is sent from neurons in SC to the burst neurons in the brainstem reticular formation (also referred to as the burst generator). This pathway is gated by tonic inhibition from the OPNs under normal conditions. Approximately 20 ms before saccade onset, OPN activity pauses, disinhibiting the burst neurons and allowing the excitatory pathway (green arrows) to actuate an eye movement. This study tests whether disinhibiting the pathway downstream of SC by blink-induced suppression of OPNs results in an immediate eye movement.