The superficial gray layer of the superior colliculus contains a map that represents the visual field, whereas the underlying intermediate gray layer contains a vector map of the saccades that shift the direction of gaze. These two maps are aligned so that a particular region of the visual field is represented directly above the neurons that orient the highest acuity area of the retina toward that region. Although it has been proposed that the transmission of information from the visuosensory to the motor map plays an important role in the generation of visually guided saccades, experiments have failed to demonstrate any functional linkage between the two layers. We examined synaptic transmission between these layers in vitro by stimulating the superficial layer while using whole- The superior colliculus receives sensory information about the location of objects and then processes this information to initiate motor command signals for the saccadic head and eye movements that orient gaze toward objects of interest (1). The proximity of these functions within the same structure makes the superior colliculus a powerful model for studying the fundamental problem of how the brain integrates sensory and motor systems to produce behavior.

Neurons in the superficial gray layer (SGS) of the superior colliculus receive visual input and excite intermediate layer (SGI) neurons that play a critical role in initiating rapid orienting movements of the eyes, called saccades. In the present study, two types of experiments demonstrate that a population of SGI neurons gives rise to a reciprocal pathway that inhibits neurons in SGS. First, in GAD67-GFP knockin mice, GABAergic SGI neurons that expressed GFP fluorescence were injected with the tracer biocytin to reveal their axonal projections. Axons arising from GFP-positive neurons in SGI terminated densely in SGS. Next, SGI neurons in rats and mice were stimulated by using the photolysis of caged glutamate, and in vitro whole-cell patch-clamp recordings were used to measure the responses evoked in SGS cells. Large, synaptically mediated outward currents were evoked in SGS neurons. These currents were blocked by gabazine, confirming that they were GABAA receptor-mediated inhibitory postsynaptic currents. This inhibitory pathway from SGI transiently suppresses visual activity in SGS, which in turn could have multiple effects. These effects could include reduction of perceptual blurring during saccades as well as prevention of eye movements that might be spuriously triggered by the sweep of the visual field across the retina.patch-clamp ͉ photostimulation ͉ sensorimotor ͉ superior colliculus ͉ visuomotor N eurons in the superficial layer (SGS) of the superior colliculus receive input from the retina and the visual cortex (1) and provide a powerful excitatory input to premotor neurons in the intermediate layer (SGI) that play a critical role in initiating rapid orienting movements of the eyes, called saccades (2-4). The activity of many of these superficial layer neurons is suppressed during saccades (5). By reducing the activity in the pathway from the superficial to the premotor cells in the intermediate layer, this suppression may prevent unwanted saccades that might otherwise be triggered by the rapid movement of the visual field that occurs during a saccade. SGS cells also project to nuclei in the dorsal thalamus that relay visual information to the cortex (1), and the reduction of activity in these relay nuclei may contribute to the attenuation of visual perception that occurs during the course of saccades (6-9).Experiments designed to identify the neural mechanisms responsible for saccadic suppression suggest that neither retinal input nor proprioceptive input from the periphery is responsible. For example, superficial layer neurons can respond to visual stimuli moving at the velocity of saccades (5), which suggests that the retinal input is suppressed after reaching SGS. Moreover, the observation that the suppression of activity in SGS can occur during eye movements in the dark indicates that the mechanism is not dependent on changes in the level of retinal activity (5). Similarly, the proposal that the suppression is mediated by input from receptors in extraocular eye muscles or tendons that detect the ...