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The objective of these experiments was to explore long-term memory in Caenorhabditis elegans. This examination of memory in a simple organism with accessible genetics and a well understood biology may permit later work to define the cellular processes that underlie long-term memory. Habituation training with a vibrational stimulus was administered on Day 1, and the retention test of a block of stimuli was given 24 h after the end of training on Day 2. Long-term retention of habituation was evident as a lower level of responding on Day 2 relative to the level of responding on Day 2 of untrained controls or the initial level of responding of worms on Day 1. In Experiments 1 and 2, a habituation training protocol that produced long-term retention of habituation was established, and the effects of stimulus number, interstimulus interval (ISI), and distribution of training on both short-term and long-term habituation were examined. In Experiment 1 (10-s ISI), there appeared to be a floor effect which resulted in a low level of responding regardless of training on Day 1; thus no evidence for long-term habituation after training at a 10-s ISI could be found. In Experiment 2 (60-s ISI), worms that received distributed and massed habituation training with 60 stimuli showed a significantly lower level of responding relative to untrained controls. The distributed habituation training appeared to be more effective at inducing long-term habituation and was used in the subsequent experiments. To characterize the effects of heat shock treatments used in the behavioral experiments that follow, the effects of heat shock on two assays, the induction of a heat shock protein gene, hsp16, and the rate of egg-laying were measured in Experiment 3. All heat shock treatments used caused the induction of hsp16. In addition, the number of eggs laid during a fixed interval after heat shock was sensitive to the heat shock treatments given in Experiments 4 through 8. In Experiments 4 through 8, the effects of heat shock on short- and long-term habituation were examined. Heat shock, which acts as a general cellular stressor, was administered at different times before, during and after training. In Experiment 4, heat shock (45 min, 32°C) was administered, ending 2 h before training on Day 1. Heat shock before training did not affect the initial level of responding on Day 1, habituation during training, short-term retention of habituation between blocks of training or long-term retention of habituation. In Experiment 5, heat shock (45 min, 32°C) was administered during the rest periods of distributed training in the 1-h interval after each training block. While heat shock during training had no significant effect on responding on Day 1, long-term habituation was blocked. In Experiment 6, the possibility that heat shock before training would prevent the disruption of long-term habituation by heat shock during training by inducing thermal tolerance was examined. This was tested by administering heat shock (45 min, 32°C) that ended 2 h before training and heat shock during training. It was found that heat shock before training did not prevent the disruption of long-term habituation by heat shock during training. In Experiment 7, the effect of heat shock that ended 2 h before the retention test on Day 2 on the retention of long-term habituation was examined. It was found that heat shock on Day 2 did not disrupt the retention of habituation. Finally, in Experiment 8, the effect of brief heat shock (15 min, 32°C) at different intervals in the rest period following the training blocks was examined in an attempt to more narrowly define a critical period for consolidation of long-term habituation. Although there was no significant effect of brief heat shock on retention of habituation, the pattern of the data suggests that there may be a period of greater vulnerability worth further investigation. In summary, heat shock given before training or before the retention test did not affect long-term habituation, while heat shock during training disrupted consolidation of long-term habituation. Taken together, these behavioral results provide the foundation for an investigation of the cellular processes underlying long-term memory in C. elegans. By exploring the dynamics of the formation of long-term habituation, intervals of time critical to the formation of long-term habituation were defined. This in turn will help to focus attention on the cellular processes whose activity during those intervals of time may be important to the consolidation of long-term memory.

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In this thesis, the author explores the connections between developments in the fields of neuroscience and neuropsychology and the theoretical study of embodiment in political and literary theory. Through examination of the development of neuroscience and its interactions with theoretical approaches to embodiment, the author argues that the current approach to interdisciplinary work in the area is limited by entrenched disciplinary boundaries. Examining how these disciplinary boundaries limit the scope of the study of cognition and embodiment presents the necessity of a new approach. Based in the work of Elizabeth A. Wilson and David Wills, the author presents a new approach, the embodied cognitive approach, as an alternative interdisciplinary approach. / Graduate / 0615

Glycine is the third most abundant of the amino acids released by muscle. Perfused rat hind-limb and sheep diaphragm preparations were employed to study the origin of glycine produced by non-ruminant and ruminant muscle. Neither the degradation of muscle and erythrocyte glutathione nor the 'leaching out' of the intracellular glycine pool contributed to the glycine released by either muscle. When the perfusions were carried out with the medium free of amino acids, the proteolysis accounted for 57% of the total glycine release by the rat hind-limb and 38% by the sheep diaphragm. Minimum de novo synthesis of glycine was 12.3 umol/3 h/30 g in the rat muscle and 10.3 umol/3 h/30 g in the sheep muscle. Addition of serine to the perfusion medium stimulated significantly both the rate of glycine efflux and total glycine production in the rat hind-limb. Similar results were obtained with the sheep diaphragm; however, the increases were not statistically significant. Addition of 5-formyl tetrahydrofolate, a specific inhibitor of serine hydroxymethyltransferase, SHMT (EC 2.1.2.1) significantly decreased the rate of glycine efflux from both the muscles. The observations using cold serine were confirmed with the experiments employing radioisotopes. Up to 40% of total glycine produced by the rat hind-limb was derived from serine, whereas in the sheep diaphragm it was only 4%. In both the muscles synthesis of glycine from serine was by SHMT and not glycine synthase (EC 2.1.2.10). Synthesis of glycine from threonine was negligible in both the muscles. SHMT activity increased in liver, diaphragm and hind-limb muscle of female rats treated with trenbolone acetate or testosterone, anabolic agents. Both the muscles incorporated 14C from (U-14C) serine and (3-14C) serine to methionine, cystine, alanine, aspartate and glutamate + glutamine. The label from (U-14C) glucose was recovered in serine and glycine in the rat hind-limb but not in the sheep diaphragm. A 'serine-glycine' cycle involving kidney and muscle is proposed. The possible significance of glycine released by muscle is discussed. Development of a system for the perfusion of sheep diaphragm with erythrocyte-free medium, and a method for the determination of radioactivity in C-2 of glycine also form a part of the thesis.

This thesis aimed to investigate the role of posterior parietal cortex (PPC) in relation to saccade planning and more specifically the spatial remapping processes essential to this behaviour. These experiments begin through the use of transcranial magnetic stimulation (TMS) on a version of the classic double-step saccade paradigm (Chapter 2). TMS was not found to disrupt spatial remapping on this task and a potential explanation for this in terms of task specifications was proposed. In Chapter 4 this theme was explored further through a series of variations on the double-step saccade task, in which the order of target presentation was manipulated; these led to the conclusion that both target encoding and spatial remapping are influenced by such task-related factors. In Chapter 3, a second set of TMS experiments is discussed, which investigated the updating of saccade plans in response to a change in target location, rather than eye position. Finally in Chapters 5 and 6 neuroimaging studies that aimed to evaluate the cortical areas involved in these processes are discussed. The first of these (Chapter 5) was an extension of the behavioural studies previously conducted in Chapter 4. The second employed a novel saccade paradigm to investigate the effect of intervening saccades made between the time of target encoding and execution (Chapter 6). The findings from these experiments supported the idea that the PPC is important for representing saccade goals and updating these following a change in the spatial relationship between the centre of gaze and the target location for a future saccade. In Chapter 7 the findings from the aforementioned studies were discussed in relation to current debate within this area of research, concerning in particular the functional significance of saccade-related neuronal activity in PPC, as were suggestions for future studies that might help provide further insight into these issues.

The aim of this thesis was to investigate cognitive recovery following closed head injury within an information processing approach. Reasons why Clinical Neuropsychology has neglected the potential contribution from experimental psychology were outlined. Relevant head injury variables were reviewed. including the cognitive deficits often associated with such damage and their recovery. A pilot study confirmed that head-injured people, even soon after injury can attempt tasks with a high information processing load. The study covered the first six months post-injury using mild/moderate and severe head-injured subjects (total n=12). the findings indicating slower performance in severe subjects and their greater susceptibility to interference from irrelevant information. The central focus of the thesis was Sternberg's Memory Scanning Paradigm and this was described in detail. The relevant literature was discussed in depth including both general and clinically-relevant studies. Although pertinent studies are scarce, brain damage appears to slow memory scanning speed, differential effects being suggested according to severity of damage. In the main study a sample of head-injured subjects (n=42) was followed-up longitudinally at 1, 3, 6, 12, 24 and 36 months post-trauma. A second patient sample (n=10) was also tested at 24 and 36 months after injury. to allow a long-term follow-up "back-up" in case of excessive drop-out. A control sample (n=10) of normal volunteers was also tested. In addition to memory scanning performance patient subjects were also tested on a number of other clinical memory tests (Rey AVLT, digit span, WMS) and subjective memory questionnaire data were also obtained. Findings pointed to a slowing of memory scanning ability after head injury, the degree of dysfunction being most marked in subjects who had sustained an extremely severe head injury. Evidence of cognitive recovery was noted in some patients beyond 12-24 month post-injury. Significant associations between memory scanning performance and other memory measures were observed and a number of clinical variables were also examained. The findings were discussed in detail and a (primarily attentional) model was proposed to describe memory scanning and its dysfunction in head injury.