Three experiments investigated the hypothesis that high doses of methylphenidate (MPH) are particularly effective in enabling boys with Attention-Deficit Hyperactivity Disorder (ADHD) to regulate the allocafion of effort and persistence under high information processing demands. In Experiment 1, the performance of boys with ADHD, ages 7 to 13, was investigated on placebo and three dosages of MPH, on a visual-memory search (VMS) task across a wide range of processing loads. Accuracy increased with dosage in a linear fashion. Findings on reaction times (RTs) revealed, however, that MPH dosage had a differential effect depending on processing load. All doses of MPH improved accuracy on low loads without a concomitant increase in processing times. When both processing load and (MPH) dosage were high, however, the ADHD boys shifted to a more cautious, time comsuming strategy, apparently in order to achieve continuing gains in accuracy. Experiment 2 compared the performance of ADHD and control boys on the VMS. It established that the ADHD group had difficulty meeting the processing demands of the VMS across all of the information loads studied, as revealed by higher error rates and slower RTs. The ADHD-control comparison also established that the effects of high doses of MPH at high loads in Experiment 1 constituted a further slowing of the ADHD boys' already slow RTs. A third, normal developmental study of boys ages 7 to 13 showed that both error rates and RTs on the VMS task decreased with age. This study also revealed considerable similarity between the performance patterns of ADHD boys and those of younger control boys on the VMS.

In a cross-sectional study we examined Iipoprotein composition and CETP mass in 15 sedentary and 12 exercising, healthy male volunteers, aged between 17-35 years. The exercising group were defined as individuals participating in at least five weekly 45 minute exercise sessions of an aerobic nature (60-85% estimated maximal oxygen uptake). The sedentary subjects were only irregularly engaged in bouts of physical activity, not more than 45 minutes per week. Seasonal data were collected: one data collection in the fall and one in the spring. A 20 day food and exercise journal was maintained during each season's data collection period. Blood lipids were measured on two and anthropometric and aerobic capacity testing were performed on 1 occasion during each season. Statistical analyses consisted of a two way ANOVA (exercise and season) to control for seasonal effects on blood lipids and Iipoprotein levels. Pearson product moment correlations were calculated between those variables that showed significant seasonal or level of activity changes. Exercising males consumed significantly greater amounts of energy (p<O.OOI), carbohydrates (p<O.OOOI), protein (p<O.OOOI), and dietary fibre (p<O.OOOI) than sedentary males; sedentary males however, consumed significantly greater amounts of alcohol than exercising males. Exercising males had significantly higher aerobic capacities and degrees of mesomorphy than sedentary subjects and exhibited significantly lower apo AI values. No differences were noted between the 2 groups in BMI, % body fat, other plasma lipids or CETP mass. In summary, regular physical activity in young, healthy male subjects was associated with increased energy and carbohydrate intake and improved aerobic capacity as compared to sedentary subjects. Moderate differences in physical activity were not however associated with alterations in plasma Iipoprotein composition or CETP concentration.

Nitric Oxide (NO) has been detected in the expiratory air of normal animals and human subjects. Recent experiments revealed that expiratory NO production rises during exercise and correlates well with O$ sb2$ consumption and heart rate. Whether or not physical conditioning influences expiratory NO output production remains unclear. In this study, NO concentration in expired gas was measured in 18 healthy male volunteers subdivided into 3 groups (sedentary, intermediate, athletes) based on their state of physical conditioning. Measurements were taken at rest and during two steady-state exercise bouts on a bicycle ergometer designed to elicit VO$ sb2$ of 1 and 2 1/min with the athletes performing an additional bout at VO$ sb2$ of 4 1/min. In the sedentary and intermediate groups, expired NO concentrations declined significantly with increasing VO$ sb2.$ In contrast, expired NO levels declined only slightly with increasing VO$ sb2$ in athletes. At a VO$ sb2$ of 2 1/min, expired NO concentrations were significantly higher in athletes compared with the other groups. When correlated with V$ rm sb{E},$ expired NO concentrations declined linearly with the increase in $ rm V sb{E}$ in sedentary and intermediate groups but not in the athletes. Only the athletes had a significant linear increase in NO output (expired NO x V$ rm sb{E})$ with increasing VO$ sb2$ (p $<$ 0.001). These results support the notion that physical conditioning increases expiratory NO output during exercise. We speculate that the rise in expiratory NO output in athletes might be due to increased vascular and/or epithelial production of NO. Enhanced vascular NO production may be the result of increased shear stress and/or upregulation of endothelial NO synthase gene expression.

No description available.

The nonrecurring-items delayed nonmatching-to-sample (DNMS) task is an integral part of contemporary monkey models of brain-damage-produced amnesia. This thesis began the development of a comparable rat model of brain-damage-produced amnesia. First, a DNMS task for rats was designed by adapting key features of the monkey task. Then, the rat DNMS task was studied in three experiments; each assessed the comparability of the rat DNMS task to the monkey DNMS task. Experiment 1 determined the rate at which the rat DNMS task is learned and the asymptotic level at which it is performed, Experiment 2 assessed the memory abilities that it taps, and Experiment 3 investigated the brain structures that are involved i n its performance. In Experiment 1, rats were trained on the DNMS task and their performance was assessed at retention delays of 4, 15, 60, 120, and 600 s. All of the rats learned the DNMS task, and their performance was comparable to that commonly reported for monkeys in terms of both the rate at which they acquired the nonmatching rule at a brief retention delay and their asymptotic accuracy at delays of up to 120 s. These results establish that rats can perform a DNMS task that closely resembles the monkey DNMS task and that they can approximate the level of performance that is achieved by monkeys. Experiment 2 examined the effects of distraction during the retention delay on the DNMS performance of rats. Rats were tested at retention delays of 60 s. On half of the trials, the rats performed a distraction task during the retention delay; on the other half, they did not. Consistent with findings from monkeys and humans, distraction during the retention delay disrupted the DNMS performance of rats. This suggests that similar memory abilities are involved in the DNMS performance of rats, monkeys, and humans. Experiment 3 investigated the effects of separate and combined bilateral lesions of the hippocampus and the amygdala on DNMS performance in pretrained rats. Rats were tested both before and after surgery at retention delays of 4, 15, 60, 120, and 600 s. Each experimental rat received bilateral lesions of the hippocampus, amygdala, or both. There were no significant differences among the three experimental groups, and the rats in each of the three experimental groups were significantly impaired, in comparison to no-surgery control rats, only at the 600-s delay. In contrast, rats that had sustained inadvertent entorhinal and perirhinal cortex damage during surgery displayed profound D N M S deficits. These results parallel the results of recent studies of the neural basis of DNMS in monkeys. They suggest that, in contrast to one previously popular view, neither the hippocampus nor the amygdala play a critical role in the DNMS of pretrained animals and that the entorhinal and perirhinal cortex are critically involved. On the basis of these findings, it appears that the rat DNMS task may prove to be a useful component of rat models of brain-damage-produced amnesia. This conclusion is supported by the preliminary results of several experiments that are currently employing the task.

This thesis was concerned with coarticulatory patterns across various speech articulators and whether these can be accounted for by similar movement organization principles. Movements of the tongue dorsum, and the upper and lower pharynx, were recorded separately by a computerized ultrasound system during the production of vowel-consonant-vowel sequences. The movement amplitude, duration, and onset (relative to specific acoustic events) were computed for each articulator for a variety of speech gestures. It was shown that both spatial and temporal aspects of the movements varied in a similar manner for the three articulators as a function of the phonological context. The results indicate that spatiotemporal articulatory adjustments for vowels co-occur with the articulation of a consonant. This pattern can be accounted for by the notions of co-production and the 'spatial proximity' hypothesis.

Recent studies have indicated stronger mood dependent memory (MDM) effects when subjects generate both the to-be-remembered events and the cues used in their retrieval, and when subjects who experience similar moods are compared to subjects who report a change in both pleasure and arousal, rather than others who report a change in pleasure alone. The first study was undertaken to experimentally evaluate the relationship between mood change and memory performance. Specifically, four mood manipulations were developed to compare memory performance in subjects assigned to no mood change, change in pleasure, change in arousal, or change in both pleasure and arousal. Subjects generated autobiographical events in response to neutral nouns, and were tested for free recall and recognition of these events two days later. Results demonstrated greater memory disruption after change in both pleasure and arousal than after change in pleasure alone. However, one-dimensional change in arousal led to as much memory disruption as did change in both dimensions. Separate ANOVAs compared each mood in combination with each other mood and indicated that MDM was more strongly supported in some combinations than others. Further, the pattern in free recall was different from the pattern in recognition indicating that MDM effects may vary interactively across moods and tasks. The second study was undertaken to validate prior research by employing subjects who experience large, but naturally occurring, changes in mood. Patients with rapid-cycling Bipolar Disorder performed a variety of tasks during study sessions and were tested for implicit and explicit memory during test sessions. Significant MDM effects were supported in free recall of autobiographical events and inkblot recognition, but not in implicit category production of autobiographical event probes, picture fragment completion, explicit nor implicit memory for letter associates. Results validate MDM as a real world phenomenon that impacts on explicit memory performance in subjects whose moods are not manipulated. Discussion centers on prospects for future studies that consider a wider range of manipulated moods and tasks, theories of emotion, and other clinical groups in the investigation of MDM.

The objective of this thesis was to test the idea that medial thalamic nuclei are part of a "memory circuit" in the brain. Rats received lesions of the anterior (ANT) or medial dorsal (MD) thalamic nuclei and were tested on two spatial tasks, a nonspatial configural task, and spontaneous and amphetamine-induced acitivity. The thalamic rats were impaired on the spatial and conifural tasks, ans some of the thalamic groups were slightly hyperactive after administration of amphertamine. The deficits were not large and could not be unequivocally attributed to the ANT or MD damage. The results question the role of the ANT or MD in the behaviors studied. It is suggested that the deficits obtained after thalamic damage may be nonspecific and it is concluded that the results do not support the notion that thalamic structures have a primary role in memory. / xi, 187 leaves : ill., plates ; 29 cm.

Previous studies in our laboratory have indicated that anesthetic block of neural activity at discrete sites within the limbic system, including the lateral hypothalamus and anterior cingulum bundle, causes a significant long-lasting analgesia during the formalin test. In this experiment, the local anesthetic lidocaine was microinjected into the dentate region of the hippocampus, an important limbic structure presumed to subserve the affective-motivational aspects of pain. The dentate gyrus is strategically situated at a point of convergence of widespread polysensory cortical input to the hippocampus, to allow modulation of cortical signals before they diverge into numerous limbic circuits. The results indicate that anesthetic block of the anterior region of the dentate gyrus produces analgesia in the rat during the formalin test. The analgesia produced by this procedure became apparent 30 minutes after regional block contralateral to the site of injury and persisted for the duration of the test period. These data provide further evidence that limbic forebrain structures are involved in pain and analgesia.

No description available.