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The experiments reported in the present dissertation investigated the contribution of the pyriform cortex and of the basolateral amygdala to three classes of affective behavior: conditioned aversions, conditioned preferences, and neophobia. It was demonstrated that lesions of the pyriform cortex cause an impairment in the acquisition of aversions to olfactory, but not gustatory, stimuli and that this impairment is not secondary to alterations in primary olfactory function. The acquisition of a preference for a particular odor paired with reward was also shown to be impaired by such lesions. These results are discussed in terms of the rich innervation of the pyriform cortex by olfactory fibers, and of its projections to sub-cortical structures. Ibotenic-acid lesions of the basolateral amygdala caused a significant deficit in conditioned taste aversion, whereas these same lesions did not affect conditioned odor aversion. This dissociation was examined in light of the differences in anatomical projections from the olfactory and gustatory cortical areas to the basolateral region. The performance of animals with electrolytic lesions of the basolateral amygdala on a conditioned taste- and a conditioned odor-preference task raised some important questions concerning the contribution of this neural structure to stimulus-reward associations. The last two experiments demonstrated that the pyriform cortex plays an important role in neophobia, a role that is not limited to olfactory stimuli. This suggests that the analysis and subsequent transmission of olfactory information is critical to the expression of the neophobic response.

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.

Thesis (M.Sc.)--University of Canterbury, 2007. / Typescript (photocopy). Includes bibliographical references (leaves 74-89). Also available via the World Wide Web.

Thesis (M.A.)--Cleveland State University, 2008. / Abstract. Title from PDF t.p. (viewed on Mar. 17, 2009). Includes bibliographical references (p.37-42) and appendices. Available online via the OhioLINK ETD Center. Also availabe in print.

Thesis (Ph.D.) - Carleton University, 2005. / Includes bibliographical references (p. 175-191). Also available in electronic format on the Internet.

Thesis (M.Sc.) - Carleton University, 2006. / Includes bibliographical references (p. 95-108). Also available in electronic format on the Internet.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 107-121).

Thesis (M.D)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 80-124) Also available in print.

Thesis (Ph. D.)--University of California, San Diego, 2006. / Title from first page of PDF file (viewed April 4, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.