The basolateral complex of the amygdala (BLA) is a key component of the neuronal circuitry underlying the acquisition and the extinction of Pavlovian conditioned fear. The present series of experiments examined the role of neuronal activity and NMDA receptors (NMDAr) activation in the BLA on learning and relearning context conditioned fear and its extinction. Disruption of neuronal activity in the BLA prevented the acquisition of fear responses to a novel, a moderately familiar or a highly familiar context. It also prevented the reacquisition of fear responses to a conditioned or an extinguished context. Local blockade of NMDAr containing the NR2B subunit prior to training extinction or re-extinction impaired the short- and long-term loss of fear responses. In contrast, a similar blockade subsequent to training extinction or re-extinction left the long-term loss of fear responses unaffected. Disruption of neuronal activity in the BLA prior to training extinction and re-extinction depressed fear responses. It impaired the long-term loss of fear produced by extinction training but spared and even facilitated the long-loss of fear produced by re-extinction training when extinction had already been learned. The exact same outcome was observed when neuronal activity in the BLA was disrupted subsequent to training extinction and re-extinction. These findings suggest that the BLA is critical for both learning and relearning context conditioned fear. In contrast, the BLA is necessary for learning but not relearning extinction of conditioned fear. This implies that once extinction has been learned, others structures support the retrieval and the expression of extinction memory. This is consistent with current neural model of extinction that involves interactions between several neural substrates including the BLA and the medial prefrontal cortex.

The experiments reported in this thesis studied the mechanisms of expression of overexpectation of conditioned fear, as measured by freezing. In Stage I, rats were conditioned to fear a tone and a flashing light conditioned stimulus (CS) through pairings with a 0.5 mA, 1 s shock. In Stage II, overexpectation was trained by the reinforcement of a compound of these CSs with a shock of the same magnitude. Two compound ?? shock pairings produced an overexpectation effect, as measured by freezing to presentations of the tone alone, while further Stage II training caused over-training of overexpectation. Expression of the overexpectation effect produced by two compound ?? shock pairings could be prevented by pre-test injection of the benzodiazepine partial inverse agonist FG7142. This effect was dose-dependent and not due to state-dependent memory. Control experiments suggested that it was also not due to any general effect of FG7142 on the Pavlovian freezing response. Freezing to a tone that had been conditioned, but not subjected to any decremental training procedures, was unaffected by administration of FG7142 before either the conditioning or test session. FG7142 also did not affect freezing to a tone that had been subjected to an associative blocking procedure. The hypothesis that overexpectation of conditioned fear may be context-dependent was also tested. However, renewal was not observed. Rats that received Stage II training in a context distinct from the Stage I training context showed equivalent expression of overexpectation regardless of whether testing was conducted in the Stage I or Stage II training context. These results are consistent with the hypothesis that overexpectation, like extinction, leads to the imposition of a GABAA receptor-mediated mask on the fear CR. Moreover, they suggest that this masking of fear is the specific consequence of negative predictive error.

Thesis (Ph. D. in Neuroscience)--Vanderbilt University, Aug. 2009. / Title from title screen. Includes bibliographical references.

Thesis (M.S.)--Ohio State University, 2008. / Title from first page of PDF file. Includes bibliographical references (p. 76-80).

Thesis (Ph. D.)--Virginia Commonwealth University, 2008. / Prepared for: Dept. of Pharmacology and Toxicology. Bibliography: leaves 153 - 179. Available online via the internet.

Thesis (M.S.)--Michigan State University. Dept. of Geological Sciences, 2008. / "Advisor, Dr. Robert L. Anstey"--Acknowledgements. "The purpose of this study is to delineate patterns of endemism in Devonian bryozoans in North America and Europe, and to suggest hypotheses for the development of biogeographic regions during the period"--Introd. Title from PDF t.p. (viewed on Aug. 4, 2009) Includes bibliographical references (p. 38-44). Also issued in print.

Thesis (Ph. D.)--Worcester Polytechnic Institute. / Keywords: program; testing; modeling; blow down; discharge; dry chemical. Includes bibliographical references (p. 364-375).

Thesis (M.A.)--University of Wisconsin--Madison, 1970. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.S.) -- Worcester Polytechnic Institute. / Keywords: TDOA; indoor geolocation; TOA. Includes bibliographical references (p.55).

Thesis (Ph. D.)--Florida State University, 2006. / Advisor: Jon Bailey, Florida State University, College of Arts and Sciences, Dept. of Psychology. Title and description from dissertation home page (viewed Sept. 13, 2006). Document formatted into pages; contains vi, 104 pages. Includes bibliographical references.