Date of Award

1-1-2017

Embargo Period

1-1-2022

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Neuroscience

College

College of Graduate Studies

First Advisor

Brett Froeliger

Second Advisor

Colleen Hanlon

Third Advisor

Jane Joseph

Fourth Advisor

Matthew Carpenter

Fifth Advisor

Thomas Jhou

Abstract

Background: Nicotine withdrawal disrupts executive function, including inhibitory control, contributing to smoking relapse. Inhibitory control and the function of its underlying corticothalamic circuitry, including the right inferior frontal gyrus (rIFG), have been recently shown to predict relapse in sated smokers. The effects of nicotine withdrawal on this relationship, however, are unknown. The primary aims of this dissertation examined the effects of smoking abstinence on the relationship between corticothalamic-mediated inhibitory control and relapse vulnerability. An exploratory aim examined the interrelationship between corticothalamic inhibitory control, laboratory lapse, and relapse for three days following a quit attempt. Methods: During two visits, following satiety and 24-hours of smoking abstinence, N = 26 smokers performed a specialized go/go/no-go (GGNG) task during fMRI-scanning and subsequently performed a laboratory lapse task in which shorter latency to smoke indicates greater relapse vulnerability. An additional cohort of N = 18 smokers were fMRI-scanned during the go/go/no-go task, completed the laboratory lapse task, and subsequently initiated a quit-attempt. Results: Poorer GGNG performance and greater rIFG BOLD signal during inhibitory control predicted shorter smoking latency independent of smoking state, with some relationships trending toward significance. Post-hoc whole brain analyses revealed a significant effect of smoking abstinence on inhibitory control BOLD signal in the right middle frontal gyrus associated with GGNG performance and smoking latency. Abstinence disrupted corticothalamic task-based functional connectivity during inhibitory control but this measure was not related to smoking behavior. Greater abstinence-induced decrements in GGNG performance predicted greater increases in smoking intensity. Consistent with prior findings among sated smokers, poorer inhibitory control and shorter laboratory smoking latency predicted, at a trend level, relapse following a quit attempt; the relationship between inhibitory control BOLD response and relapse outcomes was non-significant. Conclusions: The conclusions of this dissertation are: inhibitory control and associated brain activity in rIFG predict relapse vulnerability independent of smoking state; smoking abstinence disrupts corticothalamic functional connectivity during inhibitory control; smoking abstinence appears to disrupt proactive control and associated brain regions; inhibitory control and laboratory smoking lapse may predict cessation success.

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