| Summary: | 碩士 === 國立中央大學 === 生命科學研究所 === 95 === Tissue injury, inflammation, or ischemia usually cause an increase in local proton concentration, which is called tissue acidosis. This phenomenon often companies with disease and painful sensation. The proton has been demonstrated as the main factor of acid-induced pain. Acid-sensing ion channel 3 (ASIC3), a member of ASICs family, and vanilloid receptor 1 (VR1) are the proton-sensing receptors. Deficiency of the two genes can not completely eliminate acid–induced pain. It is possible that other molecules involved in acid–induced pain. OGR1 family that belongs to G protein-coupled receptors including ovarian cancer G protein-coupled receptor 1 (OGR1), G protein-coupled receptor 4 (GPR4), G2A, and T cell death associated gene 8 (TDAG8), has been reported as the proton-sensing receptors. The previous study in our lab has found that OGR1 family members are expressed in neuronal tissues, including dorsal root ganglion (DRG). Among these, OGR1 has the highest gene expression levels. However, whether OGR1 and GPR4 are located in nociceptors and their function in DRG remain unclear. Therefore, the objective of the thesis is to determine localization of OGR1 and GPR4 and to study their signaling pathways in primary DRG culture. I have found that OGR1 and GPR4 were mainly expressed in non-peptidergic, small-diameter nociceptors. Approximately 31%~40% of total DRG neurons contain at least two receptors of OGR1 family. A subset of OGR1 family members were co-localized with ASIC3 or VR1. In primary culture experiments, no clear conclusion was found.
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