The experiments in this thesis examined the roles of stimulus configuration on conditioned cue preference (CCP) learning by asking what information is processed and by which neural substrates. Results from Experiments 1 and 2 showed that lesions of the lateral nucleus of the amygdala (LNA) but not of fimbria-fornix (FF) impaired CCP learning when the cues paired with food during training were distinct from those not paired with food in either of two different apparatuses. In Experiments 3 and 4 LNA lesions increased the size of the CCP when the cues paired with food and no food were ambiguous in two different apparatuses. Learning the ambiguous cue CCP required at least one session of unreinforced pre-exposure to the cues and was eliminated by FF lesions. In the last series of experiments, a latent learning effect of unreinforced pre-exposure on ambiguous cue CCP learning on the radial maze was found in normal animals that received at least 3 sessions of unreinforced pre-exposure. FF lesions made before, but not after, pre-exposure eliminated the latent learning effect. Hippocampus lesions made either before or after pre-exposure eliminated the CCP learning. Taken together, the results are consistent with the hypothesis that distinct cue CCP learning is based on conditioned approach responses to cues paired with food, mediated by a neural system that includes the LNA. The results also suggest that ambiguous cue CCP learning takes place in two phases. First spatial learning occurs during unreinforced pre-exposure, a process that requires an intact FF. Subsequently, information about the location of the reinforcer is added to the spatial information during the reinforced training trials by a process of "reconsolidation". An intact hippocampus is required for this process. The implications of these results and interpretations for latent learning and latent inhibition are considered.

Eight experiments tested priming in short-term memory as a model for latent inhibition and habituation. The model postulates that the two phenomena result from reduced processing when a representation of the target stimulus is already active (primed) in short-term memory at the time of its presentation. Priming is assumed to depend on the integrity of an association formed between the contextual stimuli and the conditional stimulus (CS) during exposure. Using a procedure that should have overshadowed the context, Experiment 1 found that latent inhibition and habituation were nevertheless maintained when a second CS of either equal or shorter duration overlapped with the target during exposure. Experiment 2 found no support for the priming of a configural stimulus when simultaneous compounds were preexposed. Experiment 3 ruled out sensitization and/or pseudoconditioning as an alternative explanation of latent inhibition. Experiments 4, 5 and 6 showed that sensory preconditioning as well as habituation and latent inhibition were obtained with compound exposure, providing evidence that the added CS was indeed processed along with the target. In Experiment 7, sequential pairings produced as much latent inhibition as compounds but less sensory preconditioning. Experiment 8 showed that retardation of conditioned inhibition was not attenuated by compound exposure. These results are interpreted as consistent with a correlational approach to classical conditioning.

Thesis (Ph.D.)--University of Delaware, 2008. / Principal faculty advisor: Mark E. Stanton, Dept. of Psychology. Includes bibliographical references.

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (Ph. D.)--University of Nevada, Reno, 2008. / "December 2008." Includes bibliographical references (leaves 39-44). Online version available on the World Wide Web.

Thesis (M.S.)--State University of New York at Binghamton, Department of Psychology, 2007. / Includes bibliographical references (leaves 24-25).

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (Ph. D.)--State University of New York at Binghamton, Psychology Department, 2008. / Includes bibliographical references.

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