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Mechanisms underlying chronic pain that develops after spinal cord injury (SCI) are incompletely understood. Most research on SCI pain mechanisms has focused on neuronal alterations within pain pathways at spinal and supraspinal levels associated with inflammation and glial activation. These events might also impact central processes of primary sensory(More)
Chronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats(More)
TRPV4 (Transient Receptor Potential Vanilloid 4) channels are activated by a wide range of stimuli, including hypotonic stress, non-noxious heat and mechanical stress and some small molecule agonists (e.g. phorbol ester 4α-PDD). GSK1016790A (GSK101) is a recently discovered specific small molecule agonist of TRPV4. Its effects on physical determinants of(More)
Chronic neuropathic pain is often a severe and inadequately treated consequence of spinal cord injury (SCI). Recent findings suggest that SCI pain is promoted by spontaneous activity (SA) generated chronically in cell bodies of primary nociceptors in dorsal root ganglia (DRG). Many nociceptors express transient receptor potential V1 (TRPV1) channels, and in(More)
UNLABELLED Little is known about intracellular signaling mechanisms that persistently excite neurons in pain pathways. Persistent spontaneous activity (SA) generated in the cell bodies of primary nociceptors within dorsal root ganglia (DRG) has been found to make major contributions to chronic pain in a rat model of spinal cord injury (SCI) (Bedi et al.,(More)
Acknowledgements I would like to take this opportunity to give my sincere thanks to my advisors, Dr. Barry James, and Dr. Kang James, for their support and guidance, which make it possible for me to finish the project on time. Thanks also to Dr. Bruce Peckham for being on my committee, and all three courses I took from him. I would also like to thank our(More)
Mechanisms underlying chronic pain that develops after spinal cord injury (SCI) are incompletely understood. Most research on SCI pain mechanisms has focused on neuronal alterations within pain pathways at spinal and supraspinal levels associated with inflammation and glial activation. These events might also impact central processes of primary sensory(More)
A majority of people who have sustained spinal cord injury (SCI) experience chronic pain after injury, and this pain is highly resistant to available treatments. Contusive SCI in rats at T10 results in hyperexcitability of primary sensory neurons, which contributes to chronic pain. KCNQ channels are widely expressed in nociceptive dorsal root ganglion (DRG)(More)
iii Acknowledgements I would like to thank my advisors, Dr Edgar T. Walters, for giving me the opportunity to be trained in a scientific field which expanded my view and knowledge, for giving guidance and freedom to pursue my research interests, for helping me revise my writing again and again in spite of his tremendous workload. Additionally, I would like(More)
We develop a Bayesian method that simultaneously registers and clusters functional data of interest. Unlike other existing methods, which often assume a simple translation in the time domain, our method uses a discrete approximation generated from the family of Dirichlet distributions to allow warping functions of great flexibility. Under this Bayesian(More)
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