@phdthesis{Thum2006,
  author    = {Thum, Andreas Stephan},
  title     = {Sugar reward learning in Drosophila : neuronal circuits in Drosophila associative olfactory learning},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-17930},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2006},
  abstract  = {Genetic intervention in the fly Drosophila melanogaster has provided strong evidence that the mushroom bodies of the insect brain act as the seat of memory traces for aversive and appetitive olfactory learning (reviewed in Heisenberg, 2003). In flies, electroshock is mainly used as negative reinforcer. Unfortunately this fact complicates a comparative consideration with other inscets as most studies use sugar as positive reinforcer. For example, several lines of evidence from honeybee and moth have suggested another site, the antennal lobe, to house neuronal plasticity underlying appetitive olfactory memory (reviewed in Menzel, 2001; Daly et al., 2004). Because of this I focused my work mainly on appetitive olfactory learning. In the first part of my thesis, I used a novel genetic tool, the TARGET system (McGuire et al., 2003), which allows the temporally controlled expression of a given effector gene in a defined set of cells. Comparing effector genes which either block neurotransmission or ablate cells showed important differences, revealing that selection of the appropriate effector gene is critical for evaluating the function of neural circuits. In the second part, a new engram of olfactory memory in the Drosophila projection neurons is described by restoring Rutabaga adenlylate cyclase (rut-AC) activity specifically in these cells. Expression of wild-type rutabaga in the projection neurons fully rescued the defect in sugar reward memory, but not in aversive electric shock memory. No difference was found in the stability of the appetitive memories rescued either in projection neurons or Kenyon cells. In the third part of the thesis I tried to understand how the reinforcing signals for sugar reward are internally represented. In the bee Hammer (1993) described a single octopaminergic neuron - called VUMmx1 - that mediates the sugar stimulus in associative olfactory reward learning. Analysis of single VUM neurons in the fly (Selcho, 2006) identified a neuron with a similar morphology as the VUMmx1 neuron. As there is a mutant in Drosophila lacking the last enzymatic step in octopamine synthesis (Monastirioti et al., 1996), Tyramine beta Hydroxylase, I was able to show that local Tyramine beta Hydroxylase expression successfully rescued sugar reward learning. This allows to conclude that about 250 cells including the VUM cluster are sufficient for mediating the sugar reinforcement signal in the fly. The description of a VUMmx1 similar neuron and the involvement of the VUM cluster in mediating the octopaminergic sugar stimulus are the first steps in establishing a neuronal map for US processing in Drosophila. Based on this work several experiments are contrivable to reach this ultimate goal in the fly. Taken together, the described similiarities between Drosophila and honeybee regarding the memory organisation in MBs and PNs and the proposed internal representation of the sugar reward suggest an evolutionarily conserved mechanism for appetitive olfactory learning in insects.},
  subject      = {Taufliege},
  language  = {en}
}
@techreport{MagnusLinkerMeuthetal.2011,
  author    = {Magnus, Tim and Linker, Ralf A. and Meuth, Sven G. and Kleinschnitz, Christoph and Korn, Thomas},
  title     = {Report on the 2nd scientific meeting of the "Verein zur Foerderung des Wissenschaftlichen Nachwuchses in der Neurologie" (NEUROWIND e.V.) held in Motzen, Germany, Oct. 29'th - Oct. 31'st, 2010},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68789},
  year      = {2011},
  abstract  = {Summary of the scientific contributions to the NEUROWIND meeting 2010: Contributions in the fields of neuroimmunology and neurodegeneration},
  subject      = {Wissenschaftlicher Nachwuchs},
  language  = {en}
}
@phdthesis{Hartmann2017,
  author    = {Hartmann, Jasmin},
  title     = {Neuroprotektion in der Fr{\"u}hphase nach Subarachnoidalblutung: Untersuchung potenzieller Therapieformen im Tiermodell},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-153936},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2017},
  abstract  = {Ausgehend von der Hypothese, dass die in dieser Arbeit eingesetzten Substanzen Natriumnitroprussid, Magnesium und Clazosentan aus pathophysiologischen {\"U}berlegungen dem in der Fr{\"u}hphase nach SAB auftretenden Perfusionsdefizit entgegenwirken und neuroprotektive Wirkung entfalten k{\"o}nnen, hat diese Arbeit das Ziel verfolgt, konkrete Therapieans{\"a}tze zu entwickeln, die f{\"u}r die Behandlung der fr{\"u}hen Durchblutungsst{\"o}rung nach einer SAB geeignet sein k{\"o}nnten. Ebenso sollte das neuroprotektive Potenzial dieser Substanzen, bei denen es sich um klinisch bereits getestete Medikamente handelt, evaluiert werden. Hierzu wurden drei Versuchsreihen unternommen, die folgende Ergebnisse erbrachten: Die Gabe des NO-Donators Natriumnitroprussid erwies sich als die zerebrale Perfusion in der Fr{\"u}hphase nach SAB signifikant steigernd. Damit einhergehend zeigte sich eine signifikante Reduktion der neuronalen Sch{\"a}digung im Hippocampus. Insgesamt legt diese Arbeit also das therapeutische Potential dieser Substanz f{\"u}r die Fr{\"u}hphase nach SAB nahe. F{\"u}r Magnesium konnte im Rahmen dieser Arbeit kein perfusionssteigernder Effekt festgestellt werden. Die hier erhobenen Daten weisen allerdings auf ein m{\"o}gliches neuroprotektives Potential dieser Substanz hin, sodass weitere Studien gr{\"o}ßeren Umfangs angestrebt werden sollten, um eine neuroprotektive Wirkung verifizieren zu k{\"o}nnen. Von dem ETA-Antagonisten Clazosentan wurden drei Dosierungen auf ihr neuroprotektives und perfusionssteigerndes Potential hin getestet. Hinsichtlich des perfusionssteigernden Effektes erwies sich die Maximaldosis zwar als deutlich {\"u}berlegen, verfehlte jedoch zu den Zeitpunkten 120, 150 und 180 Minuten nach SAB knapp das Signifikanzniveau. Ein neuroprotektives Potential kann auf Grundlage einer knappen Signifikanz in der H\&E-F{\"a}rbung vermutet, aber nicht sicher konstatiert, werden. Das Ziel dieses gr{\"o}ßer angelegten Projekts ist die Entwicklung einer Kombinationstherapie aus unterschiedlichen Methoden und Medikamenten. Basierend auf den hier vorgestellten Ergebnissen kommen von den in dieser Arbeit untersuchten Substanzen insbesondere der NO-Donator Natriumnitroprussid, aber auch der ETA-Antagonist Clazosentan in Frage. Als m{\"o}gliche Kombinationspartner k{\"o}nnten Prostazyklin-Agonisten oder Thrombozytenaggregationshemmer eingesetzt werden. Daneben sind die Anwendung einer moderaten Hypothermie sowie die Gabe hyperonkotischer L{\"o}sungen therapeutische Ans{\"a}tze, die im weiteren Verlauf dieses Projekts untersucht werden.},
  subject      = {Neurochirurgie},
  language  = {de}
}
@article{FranzekSperlingStoeberetal.1993,
  author    = {Franzek, E. and Sperling, W. and St{\"o}ber, Gerald and Beckmann, H.},
  title     = {Die fr{\"u}hkindliche Form einer negativistischen Katatonie},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-78448},
  year      = {1993},
  abstract  = {Es wird ein Krankheitsbild negativistischer Katatonie nach Leonhard mit nachweislichem Beginn in der fr{\"u}hen Kindheit beschrieben. Dieses zeichnet sich durch Negativismus, negativistische Erregungen mit (Auto)aggressivit{\"a}t und triebhaften Durchbr{\"u}chen aus. Die expressive Sprachentwicklung fehlt oder sie bleibt auf dem erreichten Entwicklungsstand stehen. Die k{\"o}rperliche Gesamtreifung ist retardiert. Zumeist nicht als fr{\"u}hkindliche Katatonien erkannt, werden diese Krankheiten f{\"a}lschlich als "Schwachsinn bei fr{\"u}hkindlichem Hirnschaden" oder unspezifisch als "tiefgreifende Entwicklungsst{\"o}rung" (DSM III-R, ICD 10) diagnostiziert.},
  subject      = {Schizophrenie},
  language  = {de}
}
@phdthesis{Foley2001,
  author    = {Foley, Paul Bernard},
  title     = {Beans, roots and leaves},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-1181975},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2001},
  abstract  = {The author presents the first detailed review of the pharmacological therapy of parkinsonism from ancient times until the near present (1980). It is not clear whether parkinsonism as it is now defined - a progressive neurodegenerative disorder of the basal ganglia characterized by sharply reduced striatal dopamine levels, particularly in the striatum - has always affected a significant minority of aged persons, but suggestive evidence to this effect in the older literature is reviewed. The major discussion commences, however, with the administration of various plant alkaloids to parkinsonian patients in the second half of the 19th century. Antiparkinsonian therapy since this time may be divided into a number of phases: 1. The employment of alkaloids derived from solanaceous plants: initially hyoscyamine, then hyoscine/scopolamine and atropine. The discovery and characterization of these alkaloids, and the gradual recognition that other pharmacologically useful solanaceous alkaloids (such as duboisine) were identical with one or other of these three compounds, is discussed. 2. With the outbreak of encephalitis lethargica following the First World War, parkinsonian patient numbers increased dramatically, leading to a multiplicity of new directions, including the use of another solanaceous plant, stramonium, of extremely high atropine doses, and of harmala alkaloids. 3. The so-called "Bulgarian treatment" was popularized in western Europe in the mid-1930s. It was also a belladonna alkaloid-based therapy, but associated with greater efficacy and fewer side effects. This approach, whether as actual plant extracts or as defined combinations of belladonna alkaloids, remained internationally dominant until the end of the 1940s. 4. Synthetic antiparkinsonian agents were examined following the Second World War, with the aim of overcoming the deficiencies of belladonna alkaloid therapy. These agents fell into two major classes: synthetic anticholinergic (= antimuscarinic) agents, such as benzhexol, and antihistaminergic drugs, including diphenhydramine. These agents were regarded as more effective than plant-based remedies, but certainly not as cures for the disease. 5. A complete change in direction was heralded by the discovery in 1960 of the striatal dopamine deficit in parkinsonism. This led to the introduction of L-DOPA therapy for parkinsonism, the first approach directed against an identified physiological abnormality in the disorder. 6. Subsequent developments have thus far concentrated on refinement or supplementation of the L-DOPA effect. Recent attempts to develop neuroprotective or -restorative approaches are also briefly discussed. The thesis also discusses the mechanisms by which the various types of antiparkinsonian agent achieved their effects, and also the problems confronting workers at various periods in the design and assessment of novel agents. The impact of attitudes regarding the etiology and nature of parkinsonism, particularly with regard to symptomatology, is also considered. Finally, the history of antiparkinsonian therapy is discussed in context of the general development of both clinical neurology and fundamental anatomical, physiological and biochemical research. In particular, the deepening understanding of the neurochemical basis of central nervous system function is emphasized, for which reason the history of dopamine research is discussed in some detail. This history of antiparkinsonian therapy also illustrates the fact that the nature of experimental clinical pharmacology has markedly changed throughout this period: No longer the preserve of individual physicians, it is now based firmly on fundamental laboratory research, the clinical relevance of which is not always immediately apparent, and which is only later examined in (large scale) clinical trials. It is concluded that antiparkinsonian therapy was never irrational or without basis, but has always been necessarily rooted in current knowledge regarding neural and muscular function. The achievements of L-DOPA therapy, the first successful pharmacological treatment for a neurodegenerative disorder, derived from the fruitful union of the skills and contributions of different types by laboratory scientists, pharmacologists and clinicians.},
  subject      = {Parkinson-Krankheit},
  language  = {en}
}
@phdthesis{Ebinger2005,
  author    = {Ebinger, Martin},
  title     = {Neuroph{\"a}nomenologie: Ein Oxymoron als L{\"u}ckenf{\"u}ller. Die Transformation der Ph{\"a}nomenologie durch Francisco J. Varela - eine Deformation?},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-12034},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2005},
  abstract  = {Neuroph{\"a}nomenologie ist der Versuch des Neurobiologen Francisco J. Varela seine eigene Disziplin mit der Ph{\"a}nomenologie zu verkn{\"u}pfen. Anhand einer kritischen, vergleichenden Textanalyse wird in der vorliegenden Arbeit die Legitimit{\"a}t Varelas R{\"u}ckbeziehung auf Husserl {\"u}berpr{\"u}ft. Als Pr{\"u}fsteine dienen die Begriffe "Leib", "ph{\"a}nomenologische Reduktion" und Zeitbewusstsein".},
  subject      = {Neurologie},
  language  = {de}
}