We explored the nature and time course of effects generated by spatially uninformative peripheral cues by measuring these effects with localization responses to peripheral onsets or central arrow targets. In Experiment 1, participants made saccadic eye movements to equiprobable peripheral and central targets. At short cue-target onset asynchronies (CTOAs), responses to cued peripheral stimuli suffered from slowed responding attributable to sensory adaptation while responses to central targets were transiently facilitated, presumably due to cue-elicited oculomotor activation. At the longest CTOA, saccadic responses to central and peripheral targets were indistinguishably delayed, suggesting a common, output/decision effect (inhibition of return; IOR). In Experiment 2, we tested the hypothesis that the generation of this output effect is dependent on the activation state of the oculomotor system by forbidding eye movements and requiring keypress responses to frequent peripheral targets, while probing oculomotor behavior with saccades to infrequent central arrow targets. As predicted, saccades to central arrow targets showed neither the early facilitation nor later inhibitory effects that were robust in Experiment 1. At the long CTOA, manual responses to cued peripheral targets showed the typical delayed responses usually attributed to IOR. We recommend that this late "inhibitory" cueing effect (ICE) be distinguished from IOR because it lacks the cause (oculomotor activation) and effect (response bias) attributed to IOR when it was named by Posner, Rafal, Choate, and Vaughan (1985).
Inhibition of return (IOR) operationalizes a behavioral phenomenon characterized by slower responding to cued, relative to uncued, targets. Two independent forms of IOR have been theorized: input-based IOR occurs when the oculomotor system is quiescent, while output-based IOR occurs when the oculomotor system is engaged. EEG studies forbidding eye movements have demonstrated that reductions of target-elicited P1 components are correlated with IOR magnitude, but when eye movements occur, P1 effects bear no relationship to behavior. We expand on this work by adapting the cueing paradigm and recording event-related potentials: IOR is caused by oculomotor responses to central arrows or peripheral onsets and measured by key presses to peripheral targets. Behavioral IOR is observed in both conditions, but P1 reductions are absent in the central arrow condition. By contrast, arrow and peripheral cues enhance Nd, especially over contralateral electrode sites.