The deeper layers of the superior colliculus are involved in the initiation and execution of saccadic (high velocity) eye movements. A large population of coarsely tuned collicular neurons is active before each saccade. The mechanisms by which the signals that precisely control the direction and amplitude of a saccade are extracted from the activity of the population are unknown. It has been assumed that the exact trajectory of a saccade is determined by the activity of the entire population and that information is not extracted from only the most active cells in the population at a subsequent stage of neural processing. The trajectory of a saccade could be based on vector summation of the movement tendencies provided by each member of the population of active neurons or be determined by a weighted average of the vector contributions of each neuron in the active population. Here we present the results of experiments in which a small subset of the active population was reversibly deactivated with lidocaine. These results are consistent with the predictions of the latter population-averaging hypothesis and support the general idea that the direction, amplitude and velocity of saccadic eye movements are based on the responses of the entire population of cells active before a saccadic eye movement.

Neural mechanisms underlying the initiation of saccadic eye movements were studied by recording the activity of neurons in the superior colliculus of rhesus monkeys that had extensive experience on the gap task using targets restricted to one visual field. The superposition of visual activation upon the increased excitability occurring on gap trials facilitates the occurrence of a motor burst with extremely short latency; the motor burst is tightly coupled to saccade onset for the full range of saccadic reactions times, both regular and express. We found no evidence that express saccades are a special class of saccades triggered directly by visual responses. The low frequency activity, necessary for the occurrence of express saccades, neither initiates express saccades nor serves as an accurate predictor of the direction or latency of saccades. Based upon these findings, the hypothesis that the motor burst of collicular neurons serves as a signal for triggering saccade onset can now be extended to express saccades.

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Anterograde tracing with Phaseolus vulgaris leucoagglutinin (PHA-L) was employed to describe the projection from the superficial to the deep layers of the hamster's superior colliculus (SC). Deposits of PHA-L in the stratum griseum superficiale (SGS) resulted in labelled terminal swellings in the stratum opticum and all of the deep laminae (the stratum griseum intermediate [SGI], stratum albumin intermedium [SAI], stratum griseum profundum [SGP], and stratum albumin profundum [SAP]). Labelled terminals were also visible in the periaqueductal gray (PAG). Reconstructions of individual axons showed that many collateral in the deep laminae arose from axons that projected to targets outside the colliculus. The projection from the superficial to the deep laminae had a loose topographic organization, and the trajectories of interlaminar axons were generally deflected laterally from "projection" lines that were orthogonal to the SC surface. Physiological recording and receptive field mapping were used to determine actual projection lines, which connect neurons in the superficial and deep layers that have receptive fields with the same elevation. These projection lines closely matched the trajectory of the pathway from the superficial to the deep laminae.