This thesis mainly intends to study and reach some conclusions related to major challenges concerning vocabulary teaching or learning, how vocabulary teaching can be improved, findings obtained from the studies in order to reach that purpose and to what extend the suggested alternative vocabulary techniques are effective. It is also aimed to outline the basic insights of the mind, storage, and retrieval from the literature involving linguistics and language teaching. Based on above mentioned background knowledge, it is also intended to derive some significant conclusions to improve the effectiveness and thus the quality of vocabulary teaching in language instruction. In accordance with the principles of the human memory, how we can alter current vocabulary instruction techniques and activities and what scholars offer language teachers and learners are dealt with in detail. So as to validate and prove the efficiency of suggested techniques and activities, a case study is carried out and findings are discussed at large. Additionally, interviews about vocabulary teaching have been carried out with the involved students and instructors and the obtained data has been evaluated. In the final part of the research, some implications and suggestion related to vocabulary teaching are provided along with the underlying rationale behind them aiming to increase the quality of teaching of lexical items and as a result to increase overall quality of language instruction.

The aim of the present study was to elucidate the possible relationship between the levels of various brain fatty acids and learning indices in aged and young mice classified as &ldquo / good&rdquo / or &ldquo / poor&rdquo / learners basing on their performance in a spatial learning task, the Morris Water Maze. The levels of several fatty acids including palmitic, stearic, oleic, linoleic, arachidonic acid (AA) and docosahexaenoic acid (DHA) were measured using gas chromatography separately in samples from four different brain areas: hippocampus, cortex, striatum and hypothalamus. The level of oleic acid in the cerebral cortex was significantly higher in young-good learners as compared to young-poor learners and higher in young-poor learners than in old-poor learners, with no significant difference in the concentration of this acid between old-good and old-poor learners. The most consistent correlation between animals&rsquo / learning capacity and brain fatty acid&rsquo / level was found for the arachidonic acid in the hippocampal region: AA level was significantly lower in young-good learners as compared to both young-poor learners&rdquo / and old-good learners&rdquo / with young-good learners showing significantly better performance than the two other groups. Interestingly, except hypothalamus, no significant between-group differences were recorded for the remaining fatty acids including DHA, in none of the four brain regions examined.

Probability learning is the ability to establish a relationship between stimulus and outcomes based on occurrence probabilities using repetitive feedbacks. Participants learn the task according to the cue-outcome relationship, and try to gain in depth understanding of this relationship throughout the experiment. While learning is at the highest level, people rely on their working memory. In this study 20 participants were presented a probability learning task, and their prefrontal cortex activity was measured with functional Near-Infrared Spectroscopy. It was hypothesized that as participants gain more knowledge of the probabilities they will learn cue-outcome relationships and therefore rely less on their working memory. Therefore as learning precedes a drop in the fNIRS signal is expected. We obtained results confirming our hypothesis: Significant negative correlation between dorsolateral prefrontal cortex activity and learning was found. Similarly, response time also decreased through the task, indicating that as learning precedes participants made decisions faster. Participants used either the frequency matching or the maximization strategy in order to solve the task in which they had to decide whether the blue or the red color was winning. When they use the frequency matching strategy they chose blue at the rate of winning for the blue choice. When they use the maximization strategy they chosed blue almost always. Our task was designed such that the frequency for blue to win was 80%. We had hypothesized that the people in frequency matching and maximization groups would show working memory differences which could be observed from the fNIRS signal. However, we were unable to detect this type of behavioral difference in the fNIRS signal. Overall, our study showed the relationship between probability learning and working memory as depicted by brain activity in the dorsolateral prefrontal cortex which widely known as the central executive component of working memory.

Title from title page of PDF (University of Missouri--St. Louis, viewed February 24, 2010). Includes bibliographical references (p. 29-30).

It is now well accepted, through the use of mutational studies, that genes influence behavioural variation. However, we have little knowledge of the cellular and neuronal mechanisms underlying the effects of specific genes. This thesis broadens our understanding of the neurogenetic underpinnings of naturally occurring differences in behaviour using the genetically tractable model organism Drosophila melanogaster. The thesis focuses on allelic variation at the foraging (for) gene which influences both larval and adult behaviour. In particular, for’s cellular/neural contributions to food-related behaviours and learning and memory is investigated. In the first study, we map FOR protein distribution patterns in the adult brain and use this knowledge to demonstrate a neural-specific function for the for gene in adult food-related behaviour. In the second study we demonstrate a novel role for for in the regulation of naturally existing differences in fly learning and memory in the mushroom bodies of the fly brain. In the third study, I explore FOR distribution patterns in larval tissues. I show that FOR is expressed both in neural and non-neural tissues suggesting a distributed function for FOR in food-related behaviours in the larva. In the last study, I describe naturally existing differences in fat metabolism in the Drosophila larva fat storage tissue. FOR is expressed in the fat storage tissue and may regulate lipid packaging, a trait linked to foraging. In general, my thesis is a cellular and neurogenetic analysis of natural variation in behavioural and physiological traits of D. melanogaster. The functions of FOR in food-related behaviours, nutrient physiology and cognition are conserved across taxa. The findings of this thesis should provide a framework to understand these phenomena in a wide range of organisms.

It is now well accepted, through the use of mutational studies, that genes influence behavioural variation. However, we have little knowledge of the cellular and neuronal mechanisms underlying the effects of specific genes. This thesis broadens our understanding of the neurogenetic underpinnings of naturally occurring differences in behaviour using the genetically tractable model organism Drosophila melanogaster. The thesis focuses on allelic variation at the foraging (for) gene which influences both larval and adult behaviour. In particular, for’s cellular/neural contributions to food-related behaviours and learning and memory is investigated. In the first study, we map FOR protein distribution patterns in the adult brain and use this knowledge to demonstrate a neural-specific function for the for gene in adult food-related behaviour. In the second study we demonstrate a novel role for for in the regulation of naturally existing differences in fly learning and memory in the mushroom bodies of the fly brain. In the third study, I explore FOR distribution patterns in larval tissues. I show that FOR is expressed both in neural and non-neural tissues suggesting a distributed function for FOR in food-related behaviours in the larva. In the last study, I describe naturally existing differences in fat metabolism in the Drosophila larva fat storage tissue. FOR is expressed in the fat storage tissue and may regulate lipid packaging, a trait linked to foraging. In general, my thesis is a cellular and neurogenetic analysis of natural variation in behavioural and physiological traits of D. melanogaster. The functions of FOR in food-related behaviours, nutrient physiology and cognition are conserved across taxa. The findings of this thesis should provide a framework to understand these phenomena in a wide range of organisms.

The mammalian genome encodes five collapsin response mediator protein (CRMP) isoforms. Cell culture studies have shown that the CRMPs mediate growth cone dynamics and neuron polarity through associations with a variety of signal transduction components and cytoskeletal elements. CRMP is also a member of a protein family including the presumably ancestral dihydropyrimidinase (DHP) protein that catalyzes the second step in pyrimidine degradation. In Drosophila, CRMP and DHP proteins are produced by alternatively spliced transcripts of the CRMP gene. The alternative protein forms have a 91% sequence identity, but unique expression patterns. CRMP is found exclusively in neuronal tissues and DHP is ubiquitously expressed in non-neuronal tissues. Comparative analysis of CRMP homologous sequences from insect taxa show CRMP alternative splicing is a common feature and probably represents the ancestral state of this gene family. To investigate the regulatory role of CRMP, loss-of-function mutations of CRMP that lack both proteins were isolated; homozygous animals display DHP-null phenotypes but exhibit no overt developmental or neurological defects. To determine possible interactions of Drosophila CRMP with signaling pathways in which mammalian CRMP has been shown to act, the UAS-GAL4 system was utilized. Phenotypes produced by misexpression of a variety of UAS signal transduction mediator responders were modified in a CRMP mutant background. The modification entails enhancement or suppression of a specific phenotype in a direction that corresponds to the hypothesized involvement of mammalian CRMP in signaling pathways that regulate growth cone dynamics. These data suggest that Drosophila CRMP has a role in cell signaling pathways similar to the role of the mammalian CRMPs. Furthermore, recent findings demonstrate that CRMP plays an important role in learning and memory of mice, leading to the assessment of new phenotypes in the Drosophila CRMP mutants. Tests utilizing the Pavlovian olfactory conditioning assay reveal that loss of CRMP function leads to significant learning, 3 hour memory, and long term memory deficits. Preliminary data also suggest that Drosophila CRMP may be required for normal circadian locomotor rhythms. Collectively, the data presented here demonstrate CRMP’s role in adult behavioral processes and regulating signaling events comparable to mammalian CRMP signaling.

No description available.

No description available.

We have recently established that aberrant alkylacylglycerophosphocholine metabolism results in the increased tissue concentration of platelet activating factors (PAFs) in the temporal cortex of Alzheimer Disease (AD) patients and in TgCRND8 mice over-expressing mutant human amyloid precursor protein. PAF lipids activate a G-protein coupled receptor (PAFR) reported to be expressed by microglia and subsets of neurons in rat. It is not known whether this same expression pattern is recapitulated in mice however, as the expression has only been inferred by use of pharmacological PAFR antagonists, many of which impact on both PAFR-dependent and PAFR-independent signalling pathways. PAFR plays a role in long term potentiation (LTP) induction in rats. PAFR has also been implicated in behavioural indices of spatial learning and memory in rats. Contradictory reports using mice provide ambiguity regarding the role of PAFR in LTP induction in mice. To assess whether PAFR is expressed in murine neurons, I localized PAFR mRNA in wild-type C57BL/6 mice using PAFR KO mice as a negative control. I further showed that the loss of PAFR did not impair learning and memory although this assessment must be considered preliminary as the behavioural test employed was not optimized to detect changes in learning and memory of C57BL/6 mice over time adequately.Finally, I showed that the loss of PAFR in TgCRND8 mouse model of AD had no impact upon Aβ plaque number. My observations suggest that PAFR is restricted to microglial-like cells in mouse hippocampus and as such, it may not play a role in learning and memory.