@phdthesis{Wagh2005,
  author    = {Wagh, Dhananjay Anil},
  title     = {"Bruchpilot" -molecular and functional characterization of a novel active zone protein at the Drosophila synapse},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-14989},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2005},
  abstract  = {Chemical neurotransmission is a complex process of central importance for nervous system function. It is thought to be mediated by the orchestration of hundreds of proteins for its successful execution. Several synaptic proteins have been shown to be relevant for neurotransmission and many of them are highly conserved during evolution- suggesting a universal mechanism for neurotransmission. This process has checkpoints at various places like, neurotransmitter uptake into the vesicles, relocation of the vesicles to the vicinity of calcium channels in order to facilitate Ca2+ induced release thereby modulating the fusion probability, formation of a fusion pore to release the neurotransmitter and finally reuptake of the vesicles by endocytosis. Each of these checkpoints has now become a special area of study and maintains its own importance for the understanding of the overall process. Ca2+ induced release occurs at specialized membrane structures at the synapse known as the active zones. These are highly ordered electron dense grids and are composed of several proteins which assist the synaptic vesicles in relocating in the vicinity of Ca2+ channels thereby increasing their fusion probability and then bringing about the vesicular fusion itself. All the protein modules needed for these processes are thought to be held in tight arrays at the active zones, and the functions of a few have been characterized so far at the vertebrate active zones. Our group is primarily interested in characterizing the molecular architecture of the Drosophila synapse. Due to its powerful genetics and well-established behavioural assays Drosophila is an excellent system to investigate neuronal functioning. Monoclonal antibodies (MABs) from a hybridoma library against Drosophila brain are routinely used to detect novel proteins in the brain in a reverse genetic approach. Upon identification of the protein its encoding genetic locus is characterized and a detailed investigation of its function is initiated. This approach has been particularly useful to detect synaptic proteins, which may go undetected in a forward genetic approach due to lack of an observable phenotype. Proteins like CSP, Synapsin and Sap47 have been identified and characterized using this approach so far. MAB nc82 has been one of the shortlisted antibodies from the same library and is widely used as a general neuropil marker due to the relative transparency of immunohistochemical whole mount staining obtained with this antibody. A careful observation of double stainings at the larval neuromuscular junctions with MAB nc82 and other pre and post-synaptic markers strongly suggested an active zone localization of the nc82 antigen. Synaptic architecture is well characterized in Drosophila at the ultrastructural level. However, molecular details for many synaptic components and especially for the active zone are almost entirely unknown. A possible localization at the active zone for the nc82 antigen served as the motivation to initiate its biochemical characterization and the identification of the encoding gene. In the present thesis it is shown by 2-D gel analysis and mass spectrometry that the nc82 antigen is a novel active zone protein encoded by a complex genetic locus on chromosome 2R. By RT-PCR exons from three open reading frames previously annotated as separate genes are demonstrated to give rise to a transcript of at least 5.5 kb. Northern blots produce a prominent signal of 11 kb and a weak signal of 2 kb. The protein encoded by the 5.5 kb transcript is highly conserved amongst insects and has at its N-terminus significant homology to the previously described vertebrate active zone protein ELKS/ERC/CAST. Bioinformatic analysis predicts coiled-coil domains spread all over the sequence and strongly suggest a function involved in organizing or maintaining the structure of the active zone. The large C-terminal region is highly conserved amongst the insects but has no clear homologues in veretebrates. For a functional analysis of this protein transgenic flies expressing RNAi constructs under the control of the Gal4 regulated enhancer UAS were kindly provided by the collaborating group of S.Sigrist (G\&\#1616;ttingen). A strong pan-neuronal knockdown of the nc82 antigen by transgenic RNAi expression leads to embryonic lethality. A relatively weaker RNAi expression results in behavioural deficits in adult flies including unstable flight and impaired walking behavior. Due to this peculiar phenotype as observed in the first knockdown studies the gene was named "bruchpilot" (brp) encoding the protein "Bruchpilot (BRP)" (German for crash pilot). A pan-neuronal as well as retina specific downregulation of this protein results in loss of ON and OFF transients in ERG recordings indicating dysfunctional synapses. Retina specific downregulation also shows severely impaired optomotor behaviour. Finally, at an ultrastructural level BRP downregulation seems to impair the formation of the characteristic T-shaped synaptic ribbons at the active zones without significantly altering the overall synaptic architecture (in collaboration with E.Asan). Vertebrate active zone protein Bassoon is known to be involved in attaching the synaptic ribbons to the active zones as an adapter between active zone proteins RIBEYE and ERC/CAST. A mutation in Bassoon results in a floating synaptic ribbon phenotype. No protein homologous to Bassoon has been observed in Drosophila. BRP downregulation also results in absence of attached synaptic ribbons at the active zones. This invites the speculation of an adapter like function for BRP in Drosophila. However, while Bassoon mutant mice are viable, BRP deficit in addition to the structural phenotype also results in severe behavioural and physiological anomalies and even stronger downregulation causes embryonic lethality. This therefore suggests an additional and even more important role for BRP in development and normal functioning of synapses in Drosophila and also in other insects. However, how BRP regulates synaptic transmission and which other proteins are involved in this BRP dependant pathway remains to be investigated. Such studies certainly will attract prominent attention in the future.},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Tyagi2012,
  author    = {Tyagi, Anu},
  title     = {Role of SWI/SNF in regulating pre-mRNA processing in Drosophila melanogaster},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-72253},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {ATP dependent chromatin remodeling complexes are multifactorial complexes that utilize the energy of ATP to rearrange the chromatin structure. The changes in chromatin structure lead to either increased or decreased DNA accessibility. SWI/SNF is one of such complex. The SWI/SNF complex is involved in both transcription activation and transcription repression. The ATPase subunit of SWI/SNF is called SWI2/SNF2 in yeast and Brahma, Brm, in Drosophila melanogaster. In mammals there are two paralogs of the ATPase subunit, Brm and Brg1. Recent studies have shown that the human Brm is involved in the regulation of alternative splicing. The aim of this study was to investigate the role of Brm in pre-mRNA processing. The model systems used were Chironomus tentans, well suited for in situ studies and D. melanogaster, known for its full genome information. Immunofluorescent staining of the polytene chromosome indicated that Brm protein of C. tentans, ctBrm, is associated with several gene loci including the Balbiani ring (BR) puffs. Mapping the distribution of ctBrm along the BR genes by both immuno-electron microscopy and chromatin immunoprecipitation showed that ctBrm is widely distributed along the BR genes. The results also show that a fraction of ctBrm is associated with the nascent BR pre-mRNP. Biochemical fractionation experiments confirmed the association of Brm with the RNP fractions, not only in C. tentans but also in D. melanogaster and in HeLa cells. Microarray hybridization experiments performed on S2 cells depleted of either dBrm or other SWI/SNF subunits show that Brm affects alternative splicing and 3´ end formation. These results indicated that BRM affects pre-mRNA processing as a component of SWI/SNF complexes. 1},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Triphan2009,
  author    = {Triphan, Tilman},
  title     = {The Central Control of Gap Climbing Behaviour in Drosophila melanogaster},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-43666},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {In this work, a behavioural analysis of different mutants of the fruit fly Drosophila melanogaster has been carried out. Primarily, the gap climbing behaviour (Pick \& Strauss, 2005) has been assayed as it lends itself for the investigation of decision making processes and the neuronal basis of adaptive behaviour. Furthermore it shows how basic motor actions can be combined into a complex motor behaviour. Thanks to the neurogenetic methods, Drosophila melanogaster has become an ideal study object for neurobiological questions. Two different modules of climbing control have been examined in detail. For the decision making, the mutant climbing sisyphus was analysed. While wild-type flies adapt the initiation of climbing behaviour to the width of the gap and the probability for a successful transition. climbing sisyphus flies initiate climbing behaviour even at clearly insurmountable gap widths. The climbing success itself is not improved in comparison to the wild-type siblings. The mutant climbing sisyphus is a rare example of a hyperactive mutant besides many mutants that show a reduced activity. Basic capabilities in vision have been tested in an optomotor and a distance-estimation paradigm. Since they are not affected, a defect in decision making is most probably the cause of this behavioural aberration. A second module of climbing control is keeping up orientation towards the opposite side of the gap during the execution of climbing behaviour. Mutants with a structural defect in the protocerebral bridge show abnormal climbing behaviour. During the climbing attempt, the longitudinal body axis does not necessarily point into the direction of the opposite side. Instead, many climbing events are initiated at the side edge of the walking block into the void and have no chance to ever succeed. The analysed mutants are not blind. In one of the mutants, tay bridge1 (tay1) a partial rescue attempt used to map the function in the brain succeeded such that the state of the bridge was restored. That way, a visual targeting mechanism has been activated, allowing the flies to target the opposite side. When the visibility of the opposing side was reduced, the rescued flies went back to a tay1 level of directional scatter. The results are in accord with the idea that the bridge is a central constituent of the visual targeting mechanism. The tay1 mutant was also analysed in other behavioural paradigms. A reduction in walking speed and walking activity in this mutant could be rescued by the expression of UAS-tay under the control of the 007Y-GAL4 driver line, which concomitantly restores the structure of the protocerebral bridge. The separation of bridge functions from functions of other parts of the brain of tay1 was accomplished by rescuing the reduced optomotor compensation in tay1 by the mb247-GAL4>UAS-tay driver. While still having a tay1-like protocerebral bridge, mb247-GAL4 rescue flies are able to compensate at wild-type levels. An intact compensation is not depended on the tay expression in the mushroom bodies, as mushroom body ablated flies with a tay1 background and expression of UAS-tay under the control of mb247-GAL4 show wild-type behaviour as well. The most likely substrate for the function are currently unidentified neurons in the fan-shaped body, that can be stained with 007Y-GAL4 and mb247-GAL4 as well.},
  subject      = {Taufliege},
  language  = {en}
}
@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}
}
@phdthesis{Schwaerzel2003,
  author    = {Schw{\"a}rzel, Martin},
  title     = {Localizing engrams of olfactory memories in Drosophila},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-5065},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2003},
  abstract  = {Zars and co-workers were able to localize an engram of aversive olfactory memory to the mushroom bodies of Drosophila (Zars et al., 2000). In this thesis, I followed up on this finding in two ways. Inspired by Zars et al. (2000), I first focused on the whether it would also be possible to localize memory extinction.While memory extinction is well established behaviorally, little is known about the underlying circuitry and molecular mechanisms. In extension to the findings by Zars et al (2000), I show that aversive olfactory memories remain localized to a subset of mushroom body Kenyon cells for up to 3 hours. Extinction localizes to the same set of Kenyon cells. This common localization suggests a model in which unreinforced presentations of a previously learned odorant intracellularly antagonizes the signaling cascades underlying memory formation. The second part also targets memory localization, but addresses appetitive memory. I show that memories for the same olfactory cue can be established through either sugar or electric shock reinforcement. Importantly, these memories localize to the same set of neurons within the mushroom body. Thus, the question becomes apparent how the same signal can be associated with different events. It is shown that two different monoamines are specificaly necessary for formation of either of these memories, dopamine in case of electric shock and octopamine in case of sugar memory, respectively. Taking the representation of the olfactory cue within the mushroom bodies into account, the data suggest that the two memory traces are located in the same Kenyon cells, but in separate subcellular domains, one modulated by dopamine, the other by octopamine. Taken together, this study takes two further steps in the search for the engram. (1) The result that in Drosophila olfactory learning several memories are organized within the same set of Kenyon cells is in contrast to the pessimism expressed by Lashley that is might not be possible to localize an engram. (2) Beyond localization, a possibible mechanism how several engrams about the same stimulus can be localized within the same neurons might be suggested by the models of subcellular organisation, as postulated in case of appetitive and aversive memory on the one hand and acquisition and extinction of aversive memory on the other hand.},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Schwenkert2005,
  author    = {Schwenkert, Isabell},
  title     = {Phenotypic characterization of hangover at the neuromuscular junction},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-14977},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2005},
  abstract  = {Ethanoltoleranz beruht vermutlich auf Ver{\"a}nderung in synaptischer Plastizit{\"a}t; da die Mechanismen, die zu dieser Anpassung der Synapsen f{\"u}hren, in hang-Mutanten offensichtlich defekt sind, war es Ziel dieser Arbeit zu erkl{\"a}ren, wie HANG zu synaptischer Plastizit{\"a}t beitr{\"a}gt. In diesem Zusammenhang war es besonders wichtig herauszufinden, in welchem neuronalen Prozeß HANG eine Rolle spielt. Antik{\"o}rperfarbungen gegen HANG zeigten, da das Protein in allen neuronalen Zellkernen larvaler und adulter Gehirne vorhanden ist. Gehirne der hangAE10 Mutante zeigen keine F{\"a}rbung, was best{\"a}tigt, da diese Tiere Nullmutanten f{\"u}r HANG sind. Eine genauere Analyse der Verteilung von HANG im Zellkern ergab, daß HANG in einem punktartigen Muster an bestimmten Stellen im Kern angereichert ist; diese HANG-Aggregate sind an der Innenseite der Kernmembran lokalisiert und colokalisieren nicht mit dem Chromatin. Auf der Basis dieser Ergebnissen wurde postuliert, daß HANG vermutlich an der Stabilisierung, Prozessierung oder dem Export von mRNAs beteiligt ist. Da synaptische Plastizit{\"a}t gut an den einzelnen Neuronen der neuromuskul{\"a}ren Synapse von Drosophila-Larven studiert werden kann, wurde die Morphologie der Motorneurone dritter Larven am Muskelpaar 6/7 des Segments A4 untersucht. Diese Untersuchungen zeigten, da Boutonanzahl und Axonl{\"a}nge in hangAE10-Larven um 40 \% erh{\"o}ht sind. Außerdem zeigen einige Boutons der hang-Mutanten eine abnormale, sanduhrf{\"o}rmige Form, was darauf hinweist, daß sie nach Initiation der Bouton-Teilung m{\"o}glicherweise in einem halb-separierten Zustand geblieben sind. Die Zunahme an Boutons in den Mutanten ist im wesentlichen auf eine Zunahme der Anzahl der Typ Ib-Boutons zur{\"u}ckzuf{\"u}hren. Die Analyse der Verteilung verschiedener synaptischer Marker in hangover-Mutanten ergab keine Hinweise auf Abnormalit{\"a}ten im Zytoskelett oder in der Ausbildung der pr{\"a}-und postsynaptischen Strukturen. Des weiteren ist die Anzahl der aktiven Zonen relativ zur Boutonoberfl{\"a}che nicht ver{\"a}ndert; da hang-Mutanten aber mehr synaptische Boutons pro synaptischem Terminal besitzen, kann man insgesamt von einer Zunahme der Anzahl der aktiven Zonen ausgehen. Die pr{\"a}synaptische Expression von HANG in den Mutanten rettet die erh{\"o}hte Boutonanzahl und die verl{\"a}ngerten Axone, was ebenfalls beweist, daß die beobachteten synaptischen Defekte auf das Fehlen von HANG und nicht auf Sekund{\"a}rmutationen zur{\"u}ckzuf{\"u}hren sind. Eine postsynaptische Expression der hangover cDNA in den Mutanten dagegen rettet den Ph{\"a}notyp nicht. Die Anzahl der synaptischen Boutons wird unter anderem durch cAMP-Levels bestimmt, welche somit synaptische Plastizit{\"a}t regeln. Da hang-Mutanten eine erh{\"o}hte Boutonanzahl aufweisen, f{\"u}hrte dies zu der Spekulation, daß der Ph{\"a}notyp dieser Mutanten m{\"o}glicherweise auf ver{\"a}nderte cAMPlevels zur{\"u}ckzuf{\"u}hren ist. Um dies zu {\"u}berpr{\"u}fen, wurde die Morphologie der neuromuskul{\"a}ren Synapsen von hangAE10-Larven mit denen von dnc1 verglichen, welche Defekte in der cAMP-Kaskade aufweisen. Einige Aspekte des Ph{\"a}notyps (z. B. die Zunahme der Boutonanzahl und das Verhaltnis von aktiven Zonen pro Boutonfl{\"a}che) sind sehr ¨ahnlich; jedoch unterscheiden sich die beiden Mutanten in anderen morphologischen Aspekten. Die Expression eines UAS-dnc-Transgens in hangover-Mutanten modifizierte den hang-Ph{\"a}notyp ebenfalls nicht. Auf der Basis der Ergebnisse dieser Arbeit wurde ein Modell f{\"u}r die Funktion von HANG erstellt, nach dem dieses Protein vermutlich am Isoform-spezifischen Spleißen bestimmter Transkripte beteiligt ist, deren Produkte f{\"u}r die synaptische Plastizit{\"a}t an der neuromuskul{\"a}ren Synapse ben{\"o}tigt werden.},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Schubert2019,
  author    = {Schubert, Frank Klaus},
  title     = {The circadian clock network of \(Drosophila\) \(melanogaster\)},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-157136},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2019},
  abstract  = {All living organisms need timekeeping mechanisms to track and anticipate cyclic changes in their environment. The ability to prepare for and respond to daily and seasonal changes is endowed by circadian clocks. The systemic features and molecular mechanisms that drive circadian rhythmicity are highly conserved across kingdoms. Therefore, Drosophila melanogaster with its relatively small brain (ca. 135.000 neurons) and the outstanding genetic tools that are available, is a perfect model to investigate the properties and relevance of the circadian system in a complex, but yet comprehensible organism. The last 50 years of chronobiological research in the fruit fly resulted in a deep understanding of the molecular machinery that drives circadian rhythmicity, and various histological studies revealed the neural substrate of the circadian system. However, a detailed neuroanatomical and physiological description on the single-cell level has still to be acquired. Thus, I employed a multicolor labeling approach to characterize the clock network of Drosophila melanogaster with single-cell resolution and additionally investigated the putative in- and output sites of selected neurons. To further study the functional hierarchy within the clock network and to monitor the "ticking clock" over the course of several circadian cycles, I established a method, which allows us to follow the accumulation and degradation of the core clock genes in living brain explants by the means of bioluminescence imaging of single-cells.},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Schmid2010,
  author    = {Schmid, Benjamin},
  title     = {Computational tools for the segmentation and registration of confocal brain images of Drosophila melanogaster},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-51490},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2010},
  abstract  = {Neuroanatomical data in fly brain research are mostly available as spatial gene expression patterns of genetically distinct fly strains. The Drosophila standard brain, which was developed in the past to provide a reference coordinate system, can be used to integrate these data. Working with the standard brain requires advanced image processing methods, including visualisation, segmentation and registration. The previously published VIB Protocol addressed the problem of image registration. Unfortunately, its usage was severely limited by the necessity of manually labelling a predefined set of neuropils in the brain images at hand. In this work I present novel tools to facilitate the work with the Drosophila standard brain. These tools are integrated in a well-known open-source image processing framework which can potentially serve as a common platform for image analysis in the neuroanatomical research community: ImageJ. In particular, a hardware-accelerated 3D visualisation framework was developed for ImageJ which extends its limited 3D visualisation capabilities. It is used for the development of a novel semi-automatic segmentation method, which implements automatic surface growing based on user-provided seed points. Template surfaces, incorporated with a modified variant of an active surface model, complement the segmentation. An automatic nonrigid warping algorithm is applied, based on point correspondences established through the extracted surfaces. Finally, I show how the individual steps can be fully automated, and demonstrate its application for the successful registration of fly brain images. The new tools are freely available as ImageJ plugins. I compare the results obtained by the introduced methods with the output of the VIB Protocol and conclude that our methods reduce the required effort five to ten fold. Furthermore, reproducibility and accuracy are enhanced using the proposed tools.},
  subject      = {Taufliege},
  language  = {en}
}
@phdthesis{Schleyer2012,
  author    = {Schleyer, Michael},
  title     = {Integrating past, present and future: mechanisms of a simple decision in larval Drosophila},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-78923},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {Is behaviour response or action? In this Thesis I study this question regarding a rather simple organism, the larva of the fruit fly Drosophila melanogaster. Despite its numerically simple brain and limited behavioural repertoire, it is nevertheless capable to accomplish surprisingly complex tasks. After association of an odour and a rewarding or punishing reinforcement signal, the learnt odour is able to retrieve the formed memory trace. However, the activated memory trace is not automatically turned into learned behaviour: Appetitive memory traces are behaviourally expressed only in absence of the rewarding tastant whereas aversive memory traces are behaviourally expressed in the presence of the punishing tastant. The 'decision' whether to behaviourally express a memory trace or not relies on a quantitive comparison between memory trace and current situation: only if the memory trace (after odour-sugar training) predicts a stronger sugar reward than currently present, animals show appetitive conditioned behaviour. Learned appetitive behaviour is best seen as active search for food - being pointless in the presence of (enough) food. Learned aversive behaviour, in turn, can be seen as escape from a punishment - being pointless in absence of punishment. Importantly, appetitive and aversive memory traces can be formed and retrieved independent from each other but also can, under appriate circumstances, summate to jointly organise conditioned behaviour. In contrast to learned behaviour, innate olfactory behaviour is not influenced by gustatory processing and vice versa. Thus, innate olfactory and gustatory behaviour is rather rigid and reflexive in nature, being executed almost regardless of other environmental cues. I suggest a behavioural circuit-model of chemosensory behaviour and the 'decision' process whether to behaviourally express a memory trace or not. This model reflects known components of the larval chemobehavioural circuit and provides clear hypotheses about the kinds of architecture to look for in the currently unknown parts of this circuit. The second chapter deals with gustatory perception and processing (especially of bitter substances). Quinine, the bitter tastant in tonic water and bitter lemon, is aversive for larvae, suppresses feeding behaviour and can act as aversive reinforcer in learning experiments. However, all three examined behaviours differ in their dose-effect dynamics, suggesting different molecular and cellular processing streams at some level. Innate choice behaviour, thought to be relatively reflexive and hard-wired, nevertheless can be influenced by the gustatory context. That is, attraction toward sweet tastants is decreased in presence of bitter tastants. The extent of this inhibitory effect depends on the concentration of both sweet and bitter tastant. Importantly, sweet tastants differ in their sensitivity to bitter interference, indicating a stimulus-specific mechanism. The molecular and cellular processes underlying the inhibitory effect of bitter tastants are unknown, but the behavioural results presented here provide a framework to further investigate interactions of gustatory processing streams.},
  subject      = {Lernen},
  language  = {en}
}
@phdthesis{Schindelin2005,
  author    = {Schindelin, Johannes},
  title     = {The standard brain of Drosophila melanogaster and its automatic segmentation},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-15518},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2005},
  abstract  = {In this thesis, I introduce the Virtual Brain Protocol, which facilitates applications of the Standard Brain of Drosophila melanogaster. By providing reliable and extensible tools for the handling of neuroanatomical data, this protocol simplifies and organizes the recurring tasks involved in these applications. It is demonstrated that this protocol can also be used to generate average brains, i.e. to combine recordings of several brains with the same features such that the common features are emphasized. One of the most important steps of the Virtual Insect Protocol is the aligning of newly recorded data sets with the Standard Brain. After presenting methods commonly applied in a biological or medical context to align two different recordings, it is evaluated to what extent this alignment can be automated. To that end, existing Image Processing techniques are assessed. I demonstrate that these techniques do not satisfy the requirements needed to guarantee sensible alignments between two brains. Then, I analyze what needs to be taken into account in order to formulate an algorithm which satisfies the needs of the protocol. In the last chapter, I derive such an algorithm using methods from Information Theory, which bases the technique on a solid mathematical foundation. I show how Bayesian Inference can be applied to enhance the results further. It is demonstrated that this approach yields good results on very noisy images, detecting apparent boundaries between structures. The same approach can be extended to take additional knowledge into account, e.g. the relative position of the anatomical structures and their shape. It is shown how this extension can be utilized to segment a newly recorded brain automatically.},
  subject      = {Taufliege},
  language  = {en}
}