Role of P2X receptors in inflammatory pain (with Astrazeneca Cambridge)

炎性疼痛是由炎性介质的作用产生的感觉（疼痛感测）神经元的兴奋性增加引起的。组织损伤或感染引起组织驻留的白细胞如巨噬细胞的活化，这导致炎性介质的合成和释放。该项目将研究ATP门控P2X受体离子通道在炎症性疼痛中作用的分子机制，重点关注这些通道在人类白细胞激活和感觉神经元敏化中的作用。该项目将通过与膜片钳电生理学、钙成像、流式细胞术、蛋白质组学和细胞分离技术的合作，将联合收割机新的药理学工具结合起来，以阐明炎症疼痛的分子途径，并为药物发现提供新的途径。这是一个与阿斯利康的合作项目，该项目将包括在剑桥的神经科学部门内的公司进行研究。

Inflammatory pain results from the increased excitability of sensory (pain-sensing) neurons produced by the action of inflammatory mediators. Tissue damage or infection causes activation of tissue resident leukocytes, such as macrophage, which leads to the synthesis and release of inflammatory mediators. The project will investigate the molecular mechanisms underpinning the role of ATP-gated P2X receptor ion channels in inflammatory pain, focusing of the role of these channels in the activation of human leukocytes and in the sensitisation of sensory neurons. The project will combine new pharmacological tools available through the collaboration in combination with patch-clamp electrophysiology, calcium imaging, flow cytometry, proteomics and cell isolation techniques to elucidate molecular pathways underlying inflammatory pain and offer novel routes to drug discovery. This is a collaborative project with AstraZeneca, and the project will include a research placement at the company in Cambridge within the neuroscience division.