Date of Award:

8-2013

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Psychology

Committee Chair(s)

Timothy A. Shahan

Committee

Timothy A. Shahan

Committee

Amy L. Odum

Committee

Timothy A. Gilbertson

Committee

Kerry E. Jordan

Committee

Andrew L. Samaha

Abstract

The reemergence of problem behavior (i.e., relapse) is a key concern in most behavioral interventions. Resurgence refers to the reappearance of a previously rewarded behavior when reward for an alternative behavior is also discontinued. It is especially relevant to the reappearance of problem behavior because many behavioral interventions discontinue reward for aberrant behavior while simultaneously rewarding an appropriate response.

Understanding the underlying neuropharmacology of behavioral phenomena such as resurgence is important because it helps elucidate the neural processes at the root of such behavior, and also has implications for pharmacotherapies. Existing information about the neuropharmacology of resurgence is scarce, but suggests overlap between relapse observed in the resurgence model and relapse observed in the more widely studied reinstatement and renewal models. The aim of this dissertation was to explore additional neural systems relevant to reinstatement and renewal preparations within a resurgence paradigm to assess further overlap.

The neuropharmacology of resurgence was examined in two studies via administration of two drugs that have proven effective in blocking the reemergence of behavior in reinstatement and renewal preparations. In two experiments, rats were rewarded with food for pressing a target lever in Phase I. The lever no longer produced food in Phase II, but was delivered contingent on an alterative nose poke response. Finally in Phase III, neither response produced food deliveries. Prior to Phase III sessions, separate groups of rats were injected with various doses of the dopamine D2 receptor antagonist raclopride in Experiment 1, or the α2 agonist clonidine in Experiment 2.

Both raclopride and clonidine dose-dependently attenuated the reemergence of the target lever press. However, there was evidence that raclopride may have impacted motor behavior at both doses, whereas rats treated with clonidine showed no such deficits. Raclopride also significantly impacted rate of decline of the alternative poke at both doses tested, whereas clonidine had no effect at either dose.

The results of the present studies provide additional information about the neuropharmacology of resurgence, as well as additional evidence of overlap between resurgence, reinstatement, and renewal. These results have implications regarding underlying neural mechanisms and pharmacotherapies to attenuate relapse when alternative sources of reinforcement are thinned or discontinued.

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