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The lateral septum is heavily implicated in anxiety regulation, with lesions or pharmacological inhibition of this region suppressing rats' defensive responses in various rat models of anxiety. My first objective was to explore the functional relationship between the lateral septum and its major afferent structure, the ventral hippocampus. Although these structures are extensively connected, it was not clear if they work in concert to regulate anxiety-like behaviours. This idea was tested using a pharmacological disconnection technique, whereby communication between these two structures was disabled by infusing the GABAA agonist muscimol into one side of the lateral septum and the contralateral side of the ventral hippocampus. Increases in open-arm exploration were evident when muscimol was co-infused into one side of the lateral septum and the contralateral ventral hippocampus. By contrast, open arm exploration was not altered when muscimol was co-infused into one side of the lateral septum and the ipsilateral ventral hippocampus. These results support the contention that the ventral hippocampus and the lateral septum regulate rats' open arm exploration in a serial fashion, and that this involves ipsilateral projections from the former to the latter site. My second objective was to further characterize the neuropharmacological aspects of lateral septal regulation of behavioural defence. The lateral septum contains high levels of NPY Y1 and Y2 receptor binding sites in the brain, yet little is known about their contribution in anxiety regulation at this site. Therefore, the second aim of my thesis was to characterize the contribution of NPY and its Y1 and Y2 receptor subtypes in the lateral septal regulation of anxiety in the elevated plus maze, novelty-induced suppression of feeding, and shock-probe burying tests. I determined that distinct NPY receptors differentially contribute to NPY-mediated anxiolysis in a test specific manner, with the Y1 receptor mediating NPY-induced anxiolysis in the novelty-induced suppression of feeding test, and the Y2 receptor mediating NPY13-36-induced anxiolysis in the plus-maze test. Taken together, the results from these studies reinforce the view that the regulation of anxiety involves a variety of different, yet overlapping neural processes. / Thesis (Ph.D, Neuroscience Studies) -- Queen's University, 2012-09-25 18:02:11.172

The amounts of theories that deal with naval warfare are many. Several of those are developed under the previous century when tactics and technology were in the eve of development. Many of modern thinkers within science of war often refer to older but recognized theories. The purpose of this essay is to examine if the old but recognized theories are of current interest in modern naval warfare. The questions that are used in this essay are, what is the characteristics of the war of Yom Kippur with Mahan’s offensive and Corbett’s defensive as a starting-point and are there any of the theories that are prominent. The examination is then carried out through analysing Mahan’s offensive and Corbett’s defensive. With their theories as a starting-point the characteristics of Mahan’s offensive and Corbett’s defensive are to be found within the war of Yom Kippur. The conclusions show that there are characteristics of Mahan’s offensive and Corbett’s defensive within the war of Yom Kippur. The defensive is striking on the political strategic level. The offensive is conspicuous on the military strategic and tactical level.

Thesis (doctoral)--Groningen, 1947. / "Theses": 4 p. inserted. Includes index.

Thesis (doctoral)--Groningen, 1947. / "Theses": 4 p. inserted. Includes index.

Thesis (M.A.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 204-208).

Thesis (Honors)--College of William and Mary, 2009. / Includes bibliographical references (leaves 82-87). Also available via the World Wide Web.

Thesis (M.S. in Operations Research) Naval Postgraduate School, March 1995. / Thesis advisor(s): J. N. Eagle. Includes bibliographical references. Also available online.

Thesis (M.A.)--University of Alberta, 2010. / Title from pdf file main screen (viewed May 16, 2010). "A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Arts in Humanities Computing, Dept of History and Classics". Includes bibliographical references.

Animals face frequent threats from predators and must generate appropriate behavioural responses to ensure their survival. To achieve this, they process sensory cues to correctly identify the presence and imminence of a predatory threat, and transform this information into defensive actions. However, despite much research in identifying the circuits that may be responsible for such transformations, little is known about how this occurs mechanistically. We focus on how escape behaviour in the mouse is generated from visual predatory threats, and use a combination of behavioural, neurophysiological and anatomical methods to identify the relevant neurons and understand how they perform this computation. In this work, we developed an innate decision making paradigm in which a mouse detects and assesses sensory stimuli of varying threat evidence during exploration, choosing whether to escape to a shelter, or not. The performance data in this task were best formalised with a drift-diffusion model of decision making, providing a framework to understand innate behavioural tasks in terms of evidence accumulation and boundaries. Next, we performed calcium imaging in freely-moving mice to probe for neural correlates of decision elements and flight behaviour in brain areas that we show to be necessary for the flight responses: we found that VGluT2 neurons in the deeper medial superior colliculus (dmSC) increase their activity during a repeated threatening stimulus, while VGluT2 neurons of the dorsolateral periaqueductal gray (dPAG) are silent until just before the initiation of escape, and are maximally active during escape. These results suggest that the dmSC accumulates evidence of threat which dPAG neurons threshold. This interpretation is supported by optogenetic activation of mSC-VGluT2 neurons in vivo, which recapitulates the statistics of escape probability evoked with a visual stimulus, while activation of VGluT2 neurons in the dPAG evokes an all-or-nothing escape response. Finally, using channelrhodopsin-2-assisted circuit mapping and monosynaptic viral tracing, we reveal that over half of dPAG-VGluT2 neurons receive monosynaptic connections from mSC-VGluT2 neurons with a low probability of release, allowing this synapse to act as a high-pass filter and providing a mechanism for the computation of an escape decision. These findings advance our understanding of how defensive behaviours are generated at circuit and single-cell level, and of how neurons process information in a circuit critical for implementing basic behaviours.