Role of P2X receptors in inflammatory pain (with Astrazeneca, Cambridge) (FOUNTAIN_U19CASE2)
- Research Area Bioscience for Health
- Partner The University of East Anglia (UEA)
Dr Sam Fountain -
- Application Deadline 26/11/2018
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.
We are seeking an enthusiastic and highly motivated individual to join an international recognised research group based within the state-of-the-art Biomedical Research Centre on the Norwich Research Park. The laboratory is very well funded by the BHF, BBSRC and industrial partners. We are a highly dynamic group and presentation at domestic and international conferences is encouraged. This is a collaborative project with AstraZeneca, and the project will include a research placement at the company in Cambridge within the neuroscience division.
Layhadi JA, Turner JO, Crossman DC and Fountain SJ (2018). ATP evokes Ca2+ responses and CXCL5 secretion via P2X4 receptor activation in human monocyte-derived macrophages. J Immunology.
Stokes L, Layhadi JA, Bibic L, Dhuna K, Fountain SJ (2017). P2X4 receptor function in the nervous system and current breakthroughs in pharmacology Frontiers in Pharmacology.