Matching Items (381)
Description
The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding in 1871 of the Société Nationale de Musique by Camille Saint-Saëns (1835-1921) and Romain Bussine (1830-1899) made possible the promotion of contemporary French composers. The founding of the Société des Instruments à Vent by Paul Taffanel (1844-1908) in 1879 also invigorated a new era of chamber music for wind instruments. Within this groundbreaking environment, Mélanie Hélène Bonis (pen name Mel Bonis) entered the Paris Conservatory in 1876, under the tutelage of César Franck (1822-1890). Many flutists are dismayed by the scarcity of repertoire for the instrument in the Romantic and post-Romantic traditions; they make up for this absence by borrowing the violin sonatas of Gabriel Fauré (1845-1924) and Franck. The flute and piano works of Mel Bonis help to fill this void with music composed originally for flute. Bonis was a prolific composer with over 300 works to her credit, but her works for flute and piano have not been researched or professionally recorded in the United States before the present study. Although virtually unknown today in the American flute community, Bonis's music received much acclaim from her contemporaries and deserves a prominent place in the flutist's repertoire. After a brief biographical introduction, this document examines Mel Bonis's musical style and describes in detail her six works for flute and piano while also offering performance suggestions.
ContributorsDaum, Jenna Elyse (Author) / Buck, Elizabeth (Thesis advisor) / Holbrook, Amy (Committee member) / Micklich, Albie (Committee member) / Schuring, Martin (Committee member) / Norton, Kay (Committee member) / Arizona State University (Publisher)
Created2013
ContributorsMatthews, Eyona (Performer) / Yoo, Katie Jihye (Performer) / Roubison, Ryan (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-25
ContributorsHoeckley, Stephanie (Performer) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-24
ContributorsMcClain, Katelyn (Performer) / Buringrud, Deanna (Contributor) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-31
ContributorsHur, Jiyoun (Performer) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-01
Description
To date, it has been difficult to elucidate the role of tau in learning and memory during adulthood due to developmental compensation of other microtubule associated proteins in Tau knockout (KO) mice. Here, we generated an adeno-associated virus (AAV) expressing a doxycycline (doxy)-inducible short-hairpin (sh) RNA targeted to tau, and stereotaxically and bilaterally injected 7-month-old C57BL/6 mice with either the AAV-shRNAtau or an AAV expressing a scramble shRNA sequence. Seven days after the injections, all animals were administered doxy for thirty-five days to induce expression of shRNAs, after which they were tested in the open field, rotarod and Morris water maze (MWM) to assess anxiety like behavior, motor coordination and spatial reference memory, respectively. Our results show that reducing tau in the adult hippocampus produces significant impairments in motor coordination, endurance and spatial memory. Tissue analyses shows that tau knockdown reduces hippocampal dendritic spine density and the levels of BDNF and synaptophysin, two proteins involved in memory formation and plasticity. Our approach circumvents the developmental compensation issues observed in Tau KO models and shows that reducing tau levels during adulthood impairs cognition.
ContributorsTran, An Le (Author) / Oddo, Salvatore (Thesis director) / Velazquez, Ramon (Committee member) / Roberson, Erik (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Nicotine use is an outstanding public health problem with associated social and economic consequences. Nicotine is an active alkaloid compound in tobacco and is recognized as a psychoactive drug. Preclinically, nicotine addiction and relapse can be modeled using a self-administration-reinstatement paradigm. Here, we used a nicotine self-administration and contingent cue-induced reinstatement model to examine rapid, transient synaptic plasticity (t-SP) induced by nicotine cue-triggered motivation. Although preliminary, treatment with the NMDA GluN2B subunit antagonist, ifenprodil, reduced reinstated nicotine seeking, and increased the percentage of spines with smaller head diameters. Thus, future studies are needed to fully parse out the role of NAcore GluN2B receptors in cued nicotine seeking and t-SP.
ContributorsMccallum, Joseph John (Author) / Gipson-Reichardt, Cassandra (Thesis director) / Neisewander, Janet (Committee member) / Olive, Michael Foster (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
ContributorsZaleski, Kimberly (Contributor) / Kazarian, Trevor (Performer) / Ryan, Russell (Performer) / IN2ATIVE (Performer) / ASU Library. Music Library (Publisher)
Created2018-09-28
ContributorsDelaney, Erin (Performer) / Novak, Gail (Pianist) (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-18
Description
Angelman syndrome (AS) is a neurodevelopmental disorder characterized by developmental delays, intellectual disabilities, impaired language and speech, and movement defects. Most AS cases are caused by dysfunction of a maternally-expressed E3 ubiquitin ligase (UBE3A, also known as E6 associated protein, E6-AP) in neurons. Currently, the mechanism on how loss-of-function of the enzyme influences the nervous system development remains unknown. We hypothesize that impaired metabolism of proteins, most likely those related to E6-AP substrates, may alter the developmental trajectory of neuronal structures including dendrites, spines and synaptic proteins, which leads to disrupted activity/experience-dependent synaptic plasticity and maturation. To test this hypothesis, we conducted a detailed investigation on neuronal morphology and electrophysiological properties in the prefrontal cortex (PFC) layer 5 (L5) corticostriatal pyramidal neurons (target neurons). We found smaller soma size in the maternal Ube3a deficient mice (m-/p+; 'AS' mice) at postnatal 17-19 (P17-19), P28-35 and older than 70 days (>P70), and decreased basal dendritic processes at P28-35. Surprisingly, both excitatory and inhibitory miniature postsynaptic currents (mEPSCs and mIPSCs) decreased on these neurons. These neurons also exhibited abnormalities in the local neural circuits, short-term synaptic plasticity and AMPA/NMDA ratio: the excitatory inputs from L2/3 and L5A, and inhibitory inputs from L5 significantly reduced in AS mice from P17-19; Both the release probability (Pr) and readily-releasable vesicle (RRV) pool replenishment of presynaptic neurons of the target neurons were disrupted at P17-19 and P28-35, and the change of RRV pool replenishment maintained through adulthood (>P70). The AMPA/NMDA ratio showed abnormality in the L5 corticostriatal neurons of PFC in AS mice older than P28-35, during which it decreased significantly compared to that of age-matched WT littermates. Western Blot analysis revealed that the expression level of a key regulator of the cytoskeleton system, Rho family small GTPase cell division control protein 42 homolog (cdc42), reduced significantly in the PFC of AS mice at P28-35.These impairments of synaptic transmission and short-term synaptic plasticity may account for the impaired neuronal morphology and synaptic deficits observed in the PFC target neurons, and contribute to the phenotypes in AS model mice. The present work reveals for the first time that the E6-AP deficiency influences brain function in both brain region-specific and age-dependent ways, demonstrates the functional impairment at the neural circuit level, and reveals that the presynaptic mechanisms are disrupted in AS model. These novel findings shed light on our understanding of the AS pathogenesis and inform potential novel therapeutic explorations.
ContributorsLi, Guohui (Author) / Qiu, Shenfeng (Thesis advisor) / Newbern, Jason (Committee member) / Wu, Jie (Committee member) / Vu, Eric (Committee member) / Arizona State University (Publisher)
Created2017