Date of Award:

7-2013

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Psychology

Advisor/Chair:

Timothy A. Shahan

Abstract

Resurgence refers to the reappearance of an extinguished operant behavior when reinforcement for an alternative behavior is also discontinued. It is especially relevant to the reappearance of problem behavior because many behavioral interventions discontinue reinforcement for aberrant behavior while simultaneously reinforcing an appropriate response. Existing information about the neuropharmacology of resurgence is scarce, but suggests overlap between drug seeking observed in the resurgence model and drug seeking 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 drug seeking in reinstatement and renewal preparations. In two experiments, rats earned food pellets for pressing a target lever in Phase I. In Phase II, lever pressing no longer produced food, but food was delivered contingent on an alterative nose poke response. Finally in Phase III, neither response produced food deliveries. Prior to these Phase III sessions, separate groups of rats were injected with 0, 50, or 100 mcg/kg of the dopamine D-2 receptor antagonist raclopride in Experiment 1 or 0, 20, or 40 mcg/kg of alpha-2 agonist clonidine in Experiment 2. Both doses of raclopride were effective in blocking resurgence, but there was strong evidence that the higher dose did so via motor rather than motivational impairment. Furthermore, the lower dose significantly suppressed the alternative nose poke, which suggests motor impairment, as well. Only the higher dose of clonidine blocked resurgence, but did so with no evidence of motor impairment. Raclopride significantly impacted extinction 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. The present results may also have implications regarding underlying neural mechanisms and for pharmacotherapies to attenuate relapse when alternative sources of reinforcement are thinned or discontinued.

Comments

Resurgence refers to the reappearance of an extinguished operant behavior when reinforcement for an alternative behavior is also discontinued. It is especially relevant to the reappearance of problem behavior because many behavioral interventions discontinue reinforcement for aberrant behavior while simultaneously reinforcing an appropriate response. Existing information about the neuropharmacology of resurgence is scarce, but suggests overlap between drug seeking observed in the resurgence model and drug seeking 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 drug seeking in reinstatement and renewal preparations. In two experiments, rats earned food pellets for pressing a target lever in Phase I. In Phase II, lever pressing no longer produced food, but food was delivered contingent on an alterative nose poke response. Finally in Phase III, neither response produced food deliveries. Prior to these Phase III sessions, separate groups of rats were injected with 0, 50, or 100 mcg/kg of the dopamine D-2 receptor antagonist raclopride in Experiment 1 or 0, 20, or 40 mcg/kg of alpha-2 agonist clonidine in Experiment 2. Both doses of raclopride were effective in blocking resurgence, but there was strong evidence that the higher dose did so via motor rather than motivational impairment. Furthermore, the lower dose significantly suppressed the alternative nose poke, which suggests motor impairment, as well. Only the higher dose of clonidine blocked resurgence, but did so with no evidence of motor impairment. Raclopride significantly impacted extinction 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. The present results may also have implications regarding underlying neural mechanisms and for pharmacotherapies to attenuate relapse when alternative sources of reinforcement are thinned or discontinued.

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