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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.

In the theory of the Behavioral Inhibition System (BIS), Gray and McNaughton (2000) classified events that produce or inhibit goal-directed behaviour into two affective categories: approach versus avoidance. We experience goal-conflict when approximately equal but incompatible approach and avoidance tendencies are concurrently activated. Gray and McNaughton (2000) proposed goal-conflict as a class of mechanisms separable from "simple" mechanisms: Goal-conflict effects are maximal when incompatible approach and avoidance tendencies are balanced, simple effects are maximal when either approach or avoidance tendencies predominate. Gray and McNaughton (2000) saw the hippocampus as a key nexus for resolving goal conflict by recursive amplification of the subjective value of punishment, thereby increasing avoidance tendencies. Rodent hippocampal theta (4-12 Hz) is necessary (but not sufficient) for correct and efficient transmission of hipppocampal outputs. The BIS theory is fundamentally an animal model. It is not clear if a human BIS exists in the same form. Record human hippocampal (4-12 Hz) activity from the scalp is unlikely. However, during goal-conflict resolution, cortically generated theta recorded from the scalp could be modulated by human hippocampal theta. Therefore, superficially recorded 4-12 Hz theta spectra power was used to assess if specific goal-conflict processing activity could be detected in humans. Human goal-conflict processing was assessed in four experiments: the Stop-Signal Task (SST), an existing experimental task, and three variations of a task termed "Choice", created for this thesis. Across experiments, three key conditions were created. Approach and avoidance were balanced in the intermediate condition (maximal goal-conflict). Net approach and avoidance predominated in the adjacent conditions respectively (minimal goal-conflict). Goal-conflict was assessed as the difference between activity in the intermediate condition and the average activity across the adjacent conditions (via extraction of the orthogonal quadratic trend for significance testing). Goal-conflict increased activations consistently at F8, above the right frontal cortex. Increase in task dependent goal-conflict activations were also observed at F7, Fz and F4 above the frontal cortex, and T3, T4, T5 and T6 above the temporal cortex. Activations within the human theta frequency range (4-7 Hz) were consistently detected in the Choice tasks. In the SST, activations spanned the conventional human theta (4-7 Hz) and alpha (8-12 Hz) frequencies. In the Choice tasks, higher conflict theta at T3, T5 and F8 predicted increased avoidance. Taken together, the findings support Gray and McNaugthon�s (2000) views that a) goal-conflict is a class of mechanism separable from simple approach and avoidance; b) goal-conflict processing recruits and increases cortical rhythmic activity within the same frequency range as rodent hippocampal theta (4-12 Hz); and goal-conflict is resolved by increasing the subjective value of punishment, thereby increasing avoidance tendencies. Although speculative, the current work identified a right inferior frontal gyrus neural circuit for slower, and a presupplementary motor area circuit for faster behavioral inhibition during goal-conflict resolution. These circuits are not explicit in the current BIS model.

Anxiety disorder is prevalent and costly. But its diagnosis is underdeveloped and treatment ad hoc. This could be corrected if the neural mechanisms of anxiety were known. All anxiolytic medications produce a decrease in rodent hippocampal theta rhythm - so hippocampal theta could underlie some types of anxiety. But, a review (Chapter 2) showed that ethanol and other anxiolytics increase FM-theta in the human scalp EEG and have other properties unlike hippocampal theta. The experiments in this thesis, therefore, tested for other potential homologues (Chapter 3) of hippocampal theta in the human EEG. The phase of hippocampal theta activity is reset in a working memory task and not an equivalent reference memory task in rats. Furthermore, low doses ethanol increases and high dose ethanol (and other anxiolytics) decrease theta activity. So, EEG was recorded from 15 scalp sites while participants performed non-verbal working memory and reference memory tasks before and after ethanol administration and assessed for the presence of phase-reset and ethanol-related changes in 5-7Hz and 8-11Hz spectral power (chapter 4 and 5). There was little general evidence for stimulus-induced phase-resetting of the ongoing EEG activity (Chapter 6). Increased post-stimulus synchronization in the theta frequency range was accompanied by increases in post-stimulus spectral power - suggesting that the synchronised activity was evoked rather than reset. Across 3 experiments (Chapter 7), low dose ethanol (54.5-146.6[mu]g/l) increased 5-7Hz theta, while the highest dose (307[mu]g/l) reduced task-related-increases in 5-7Hz activity. These effects were noted across electrode locations including frontal-midline sites and particularly at the beginning of the delay period. The suppression of 5-7Hz activity also coincided with an impairment in working memory performance. The dose-response curve for 5-7Hz theta was as predicted from rat hippocampal work. This particular component, linked to high working memory load or task difficulty, is a potential of homologue hippocampal theta. A clear decrease in theta with high dose ethanol, of this type, has not been reported previously. Activity in the 8-11Hz range typically increased with all doses of ethanol. It is clearly not a homologue of hippocampal theta. This is consistent with previous reports of increased alpha with high doses of ethanol - although these have been accompanied by increased, not decreased, theta. There is a potential homologue of hippocampal theta that can be detected in the human EEG (chapter 8); but the observed changes in 5-7Hz activity cannot be localised and may not be related to the hippocampus. It is clear there is more than one type of theta within the human EEG - with opposing sensitivities to ethanol. Critically, these types were detected at a single site and apparently in phase with one another. The current data, together with the previous literature, suggest that theta can be generated concurrently in distinct networks that, under specific task demands, can become coherent and so produce synchonised activity. Future studies need to test higher doses of ethanol and other anxiolytics and use different experimental paradigms to further differentiate the theta systems in the human EEG. Human EEG could be useful for differentiating sub-types of anxiety, and the choice and effectiveness of interventions delivered.

In the theory of the Behavioral Inhibition System (BIS), Gray and McNaughton (2000) classified events that produce or inhibit goal-directed behaviour into two affective categories: approach versus avoidance. We experience goal-conflict when approximately equal but incompatible approach and avoidance tendencies are concurrently activated. Gray and McNaughton (2000) proposed goal-conflict as a class of mechanisms separable from "simple" mechanisms: Goal-conflict effects are maximal when incompatible approach and avoidance tendencies are balanced, simple effects are maximal when either approach or avoidance tendencies predominate. Gray and McNaughton (2000) saw the hippocampus as a key nexus for resolving goal conflict by recursive amplification of the subjective value of punishment, thereby increasing avoidance tendencies. Rodent hippocampal theta (4-12 Hz) is necessary (but not sufficient) for correct and efficient transmission of hipppocampal outputs. The BIS theory is fundamentally an animal model. It is not clear if a human BIS exists in the same form. Record human hippocampal (4-12 Hz) activity from the scalp is unlikely. However, during goal-conflict resolution, cortically generated theta recorded from the scalp could be modulated by human hippocampal theta. Therefore, superficially recorded 4-12 Hz theta spectra power was used to assess if specific goal-conflict processing activity could be detected in humans. Human goal-conflict processing was assessed in four experiments: the Stop-Signal Task (SST), an existing experimental task, and three variations of a task termed "Choice", created for this thesis. Across experiments, three key conditions were created. Approach and avoidance were balanced in the intermediate condition (maximal goal-conflict). Net approach and avoidance predominated in the adjacent conditions respectively (minimal goal-conflict). Goal-conflict was assessed as the difference between activity in the intermediate condition and the average activity across the adjacent conditions (via extraction of the orthogonal quadratic trend for significance testing). Goal-conflict increased activations consistently at F8, above the right frontal cortex. Increase in task dependent goal-conflict activations were also observed at F7, Fz and F4 above the frontal cortex, and T3, T4, T5 and T6 above the temporal cortex. Activations within the human theta frequency range (4-7 Hz) were consistently detected in the Choice tasks. In the SST, activations spanned the conventional human theta (4-7 Hz) and alpha (8-12 Hz) frequencies. In the Choice tasks, higher conflict theta at T3, T5 and F8 predicted increased avoidance. Taken together, the findings support Gray and McNaugthon�s (2000) views that a) goal-conflict is a class of mechanism separable from simple approach and avoidance; b) goal-conflict processing recruits and increases cortical rhythmic activity within the same frequency range as rodent hippocampal theta (4-12 Hz); and goal-conflict is resolved by increasing the subjective value of punishment, thereby increasing avoidance tendencies. Although speculative, the current work identified a right inferior frontal gyrus neural circuit for slower, and a presupplementary motor area circuit for faster behavioral inhibition during goal-conflict resolution. These circuits are not explicit in the current BIS model.

Tez (Yüksek Lisans) - Süleyman Demirel Üniversitesi, Sağlık Bilimleri Enstitüsü, Biyokimya ve Klinik Biyokimya Anabilim Dalı, 2003. / Bibliyografya var.

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.)--University of Hong Kong, 2009. / Includes bibliographical references (p. 87-109). Also available in print.

Thesis (Ph.D.)--University of Alberta, 2009. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosphy, Centre for Neuroscience. Title from pdf file main screen (viewed on November 6, 2009). Includes bibliographical references.

Thesis (M.S.)--Rutgers University, 2010. / "Graduate Program in Psychology." Includes bibliographical references (p. 49-53).