Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Kinesiology

Supervisor

Dr. Matthew Heath

Abstract

An antisaccade requires suppressing a stimulus-driven prosaccade (i.e., response suppression) and remapping a target’s spatial location to its mirror-symmetrical position (i.e., vector inversion). Notably, my previous work demonstrated that the successful execution of an antisaccade selectively lengthens the reaction time (RT) of a subsequently completed prosaccade (i.e., the unidirectional prosaccade switch-cost; Weiler & Heath, 2012a; Weiler & Heath, 2012b). Thus, the objective of this dissertation was further investigate, and ultimately provide a mechanistic explanation for the unidirectional prosaccade switch-cost.

In Chapter Two, I demonstrate that the magnitude of the unidirectional prosaccade switch-cost is not dependent of the number of previously executed antisaccades. Such a finding is noteworthy as it demonstrates that antisaccades do not engender additive inhibitory effects within the oculomotor system. In Chapter Three, I demonstrate that no-go catch-trials and antisaccades impart a comparable increase in RT for subsequently completed prosaccades. In accounting for this result, I propose that the top-down process of response suppression engenders a residual inhibition of the oculomotor networks that support prosaccade planning (i.e., the oculomotor inhibition hypothesis). Notably, however, the unidirectional prosaccade switch-cost could also be attributed to a persistent activation of non-standard antisaccade task-rules (i.e., a task-set) and therefore produce a prosaccade switch-cost (i.e., task-set inertia hypothesis). The goal of the Chapter Four was to test the theoretical predictions of the aforementioned hypotheses. Notably, Chapter Four demonstrates that only antisaccade trial-types – but not prosaccades trials requiring response suppression – lengthen the RT of subsequent prosaccades. As a result I conclude that the oculomotor inhibition hypothesis cannot account for the unidirectional prosaccade switch-cost. Instead I propose that the prosaccade switch-costa is due to a persistently active task-set adopted to complete the previous antisaccade response. In Chapter Five I demonstrate that alternating from an anti- to a prosaccade does not modulate the amplitude of the P3 event related brain potential. This is a notable finding as amplitude modulation of the P3 reflects task-set updating. These electrophysiological results are directly in line with my assertion that a persistently active antisaccade task-set provides the most parsimonious account for the unidirectional prosaccade switch-cost.


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