| Summary: | 碩士 === 國立中央大學 === 生命科學研究所 === 94 === Tissue injury and inflammation often raise local proton concentration (called tissue acidosis) and accompany with painful sensations. Tissue acidosis is a dominant factor that contributes to pain. Vanilloid receptor 1 (VR1) and acid-sensing ion channel 3 (ASIC3), one member of ASIC family, are proved to be related to acid-induced pain. However, acid-induced pain is not inhibited in ASIC3 or VR1 gene deletion. Therefore it would be interesting to know whether proton-sensing GPCRs are involved in acid-induced nociception. Proton-sensing GPCRs, including ovarian cancer G-protein-coupled receptor 1 (OGR1), GPR4, G2A, and T cell death associated gene 8 (TDAG8), are originally identified as lysophospholipid receptors. Using RT-PCR and quantitative PCR, I have found that mouse OGR1, GPR4, G2A, and TDAG8 are expressed in dordal root ganglion (DRG). Among the four genes, OGR1 has the highest expression levels in DRG, suggesting that OGR1 may have a role in sensory responses. The localization of OGR1 gene in DRG neurons was examined using in situ hybridization and the results show that 35% small-diameter and 21% large-diameter neurons have OGR1 expression. Since small-diameter neurons are related to nociception, the major function of mOGR1 is probably involved in nociception. Both of proton and sphingosylphosphatidylcholine (SPC) can activate OGR1 to increase intracellular calcium concentration, and they are competitive agonists for OGR1.
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