Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 89-107). Also available in print.

Thesis (Ph. D.)--University of Virginia, 2001. / Includes bibliographical references (leaves 144-167). Also available online through Digital Dissertations.

Thesis (M. Sc.)--York University, 2002. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references. Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ71630.

The overall goals of this dissertation were 1) to understand the role that neurons in primate primary visual cortex (V1) play in the detection of small visual stimuli, and 2) to understand the quantitative relationship between the responses of individual neurons and neural population responses in V1. These goals were addressed in experiments with awake, behaving macaque monkeys using electrophysiological and imaging techniques. Initially, I employed ideal observer models to assess V1 neural detection sensitivity in a reaction-time visual detection task and found it to be comparable to the monkey's detection sensitivity. Using the same detection task, I found weak, but significant, correlations between V1 neural activity and the trial-by-trial behavior of monkeys (choice and reaction time). The conclusion of these studies is that the monkey's behavior in the detection task was likely mediated by large neural populations. Voltage-sensitive dye imaging (VSDI) is a powerful imaging technique that is well suited for assessing the link between the activity of large neural populations and behavior. VSDI measures changes in membrane potential over a cortical area of 1-2 cm² with high spatial and temporal resolutions. Using position tuning experiments with VSDI and electrophysiology, I described the relatively unknown quantitative relationships between spiking activity, the local field potential, and VSDI. These relationships were well captured by non-linear transfer functions. Lastly, these experiments also revealed important new findings about the representation of visual space by populations of neurons in V1. In particular, we resolved a long standing debate regarding the size of the cortical point image (CPI), the area of cortex activated by a single point stimulus. We found that the CPI is constant across eccentricity in parafoveal V1, suggesting that each point in space activates an approximately equivalent amount of cortical tissue. In conclusion, the results and analyses described in this dissertation contribute to our understanding of the role that neural populations in V1 play in mediating visual detection, reveal important properties of the representation of visual space by populations of neurons in V1, and provide the first analysis of the quantitative relationship between VSDI and electrophysiological signals. / text

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Rationale and hypothesis: Diabetic neuropathy involves dying back of nerve endings that reflects impairment in axonal plasticity and regenerative nerve growth. Metabolic changes in diabetes can lead to a dysregulation of hormonal mediators, such as cytokines. Thus I studied the effect of interleukin-17A (IL-17A), a proinflammatory cytokine produced by T-cells, on the phenotype of sensory neurons derived from control or diabetic rats. I hypothesized that IL-17A induces neurite outgrowth in sensory neurons through signaling pathways that enhance mitochondrial function. IL-17A can also reverse impaired nerve regeneration associated with diabetes Objectives: Determine the ability of IL-17A to enhance neurite outgrowth in cultured sensory neurons. Investigate the signalling pathways activated by IL-17A and mechanistically link to neurite outgrowth. Study the ability of IL-17A to improve mitochondrial function of sensory neurons (since axon outgrowth consumes high levels of ATP). Methodology: Cultured adult dorsal root ganglia (DRG) sensory neurons derived from age matched control or streptozotocin (STZ)-induced type 1 diabetic rats were fixed and stained for fluorescent imaging to determine total neurite outgrowth. Western blotting determined the levels of MAPK and PI-3K activation by IL-17A and for measuring levels of proteins of mitochondrial oxidative phosphorylation pathway. Mitochondrial bioenergetic function was tested in cultured DRG neurons using the Seahorse XF Analyzer. Results: I found that IL-17A (10 ng/ml; P<0.05) significantly increased total neurite outgrowth in cultures derived from both control and STZ-diabetic rat models. This enhancement was mediated by IL-17A-dependent activation of MAPK and PI-3K pathways with maximal effect at 15 minutes (P<0.05). Pharmacological blockade of one of these activated pathways led to total inhibition of neurite outgrowth. IL-17A improved mitochondrial bioenergetic function of sensory neurons. Bioenergetics function was associated with augmented expression of proteins of mitochondrial oxidative phosphorylation. Conclusion: IL-17A enhanced axonal plasticity through activation of MAPK and PI-3K pathways and was associated with augmented mitochondrial bioenergetics function in sensory neurons / October 2014

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