Date of Award

Spring 1-1-2011

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Psychology & Neuroscience

First Advisor

Yuko Munakata

Second Advisor

Marie T. Banich

Third Advisor

Tim Curran

Abstract

Response inhibition is thought to be central to the function of the frontal lobes and intimately related to all higher cognitive functions. The effortful and controlled component to response inhibition is often assumed to be the act of motoric stopping per se, such that motoric stopping can be strategically directed either at all actions (thus taking a global form) or only a subset (thus taking a more selective form). Here we challenge these core assumptions, first by offering a more viable alternative to dominant accounts of global stopping, and second by raising both empirical and computational dilemmas for dominant accounts of selective stopping. Using behavioral, neuroimaging, electroencephalographic and computational approaches, we demonstrate that the global stopping of responses does not require control mechanisms beyond those involved in detecting contexts in which old behaviors are inappropriate - in other words, the ability to monitor context in the service of goals. A computational model is used to demonstrate that these context-monitoring processes may underlie the behavioral, neuroimaging, and pharmacological phenomena of global stopping in the absence of any controlled stopping mechanisms. This work also challenges claims that more strategically selective forms of stopping are enabled by the controlled use of a slower but more response-specific stopping mechanism. We find a developmental double dissociation between the speed of stopping and its specificity, indicating that they cannot unambiguously be taken to reflect the use of a single neural mechanism. A computational model raises further challenges for extant theories of selective stopping, raising the possibility that the control mechanisms supporting this ability are not actually directed at specific responses. Together these results challenge dominant accounts of both global and selective inhibitory control, and clarify emerging debates on the frontal substrates of response inhibition, while raising novel questions about the substrates and processes that support selective stopping. More broadly, this work provides a coherent account of prefrontal cortex function across inhibitory domains, which may in turn enable both a more precise characterization of frontal disinhibitory syndromes as well as enable more targeted diagnosis and treatment of pathologies associated with response inhibition deficits.

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