Which Visual Pathways Cause Fixation-Related Inhibition?

Visual stimuli can both inhibit and activate motor mechanisms. In one well-known example, the latency of saccadic eye movements is prolonged in the presence of a fixation stimulus, relative to the case in which the fixation stimulus disappears before the target appears. This automatic sensory-motor effect, known as the gap effect or fixation-offset effect, has been associated with inhibitory connections within the superior colliculus (SC). Visual information is provided to the SC and other oculomotor areas, such as the frontal eye fields (FEF), mainly by the magnocellular geniculostriate pathway, and also by the retinotectal pathway. We tested whether signals in these pathways are necessary to create fixation-related inhibition, by using stimuli invisible to them. We found that such stimuli, visible only to short-wave–sensitive cones (S cones), do produce fixation-related inhibition (including when warning effects were equated). We also demonstrate that this fixation-related inhibition cannot be explained by residual activation of luminance pathways and must be caused by a route separate from that of luminance fixation signals. Thus there are at least two routes that cause fixation-related inhibition, and direct sensory input to the SC or FEF by the magnocellular or retinotectal pathways is not required. We discuss the implications that there may be both cortical and collicular mechanisms.

The Magnitude of the Fixation Offset Effect with Endogenously and Exogenously Controlled Saccades

Two experiments examined saccadic reaction time (RT) in response to visual targets as a function of fixation offset condition (no offset; target simultaneous with offset and 200-msec offset-target SOA) in prosaccade and antisaccade tasks. The second experiment also included a condition in which saccades were made in response to verbal commands presented auditorally. To ensure that observers were equally prepared in each condition, auditory warning tones preceded target onset on every trial. The RT reduction associated with fixation offset (FOE, or gap effect) was identical with visual targets in the prosaccade task and in response to verbal signals, strongly implicating motor, rather than sensory, mechanisms in the FOE. The FOE in the antisaccade task was significant, but it was also significantly smaller than in the other tasks. We speculate that the reduced FOE in the antisaccade task may be due to the requirement to inhibit the superior colliculus when the target directed saccadic programs are, by instruction, erroneous.