RAGE-DEPENDENT SENSITIZATION OF THORACIC SENSORY NEURONS DURING INFLAMMATORY CONDITIONS

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Date
2016-12-19Author
G Baskaran, Manoj Nair 1984-
Type
ThesisDegree Level
MastersMetadata
Show full item recordAbstract
Various airway inflammatory diseases progress as a result of chronic inflammation, specifically neurogenic inflammation. One factor known to be involved in this is RAGE. This work has established RAGE as a key mediator in LPS-induced sensitization of afferent thoracic dorsal root ganglia neurons of the upper airway in mice. This was demonstrated from electrophysiological data showing the failure of LPS to potentiate capsaicin-evoked TRPV1 currents and increase action potential generation in RAGE KO relative to wild-type thoracic neurons. Mass spectrometry analysis for protein identification represents a step forward in biochemistry, allowing to obtain a global picture of the proteins expressed in a cell, including isoforms, post-translational modifications and downstream signalling pathways.
Degree
Master of Science (M.Sc.)Department
PhysiologyProgram
PhysiologySupervisor
Campanucci, Veronica; Ianowski, JuanCommittee
Mulligan, Sean; Chlan-Fourney, Jennifer; Cayabyab, FranciscoCopyright Date
December 2016Subject
RAGE, RAGE isoforms, RAGE KO, thoracic dorsal root ganglia, LPS, airway inflammatory disease, neurogenic inflammation, sensory neuron sensitization