Lucy is a neurophysiologist with expertise in neuronal function in acute and chronic pain, particularly in arthritis. Lucy studied for her undergraduate (Dentistry BDS, Neuroscience BSc (Hons) and postgraduate (PhD, Pharmacology) degrees at the University of Edinburgh. From there she moved to a post-doctoral position at the University of California, working on several projects including tachykinin receptor expression and function (with Michael Hanley), neuronal cation-chloride co-transporters (with John Payne) and protein kinases (with Don Walsh). In 1996 she was appointed to a Lectureship at the University of Leicester, where she worked on neuronal prostaglandins in collaboration with Blair Grubb. In 1999 she moved to the Dept of Physiology, University of Bristol. She has worked on multiple projects since then including TRP channel, cyclooxygenase and galanin contributions to primary afferent nociceptor function (MRC, Arthritis Research UK funded), neuronal mechanisms in arthritic symmetry (Wellcome Trust funded), descending prostanergic facilitatory control systems (BBSRC, MRC funded, with Prof Bridget Lumb), mTOR peripheral translation mechanisms (MRC funded, with Profs Lumb and Hunt), and most recently vascular endothelial growth factors in neuroprotection and pain (funded by Diabetes UK and Arthritis Research UK).
Over the last 10 years, she has also developed a research program in human taste perception in health and disease, in collaboration with Jan Melichar, David Nutt, and Jon Potokar from the University of Bristol. In September 2013, Lucy moved to an Associate Professor position in Life Sciences at the University of Nottingham.
My research group concentrates on various aspects of neuronal signalling in chronic pain. We work towards the goal of furthering our understanding of the ways in which the nervous system responds to… read more
HULSE RP, BEAZLEY-LONG N, VED N, BESTALL SM, RIAZ H, SINGHAL P, BALLMER-HOFER K, HARPER SJ, BATES DO and DONALDSON LF, 2015. Vascular Endothelial Growth Factor (VEGF-A)165b prevents diabetic neuropathic pain and hyperglycaemia-induced sensory neuronal degeneration. Clinical Science. 129(8), 741-56 BEAZLEY-LONG, N., HUA, J., JEHLE, T., HULSE, R.P., DERSCH, R., LEHRLING, C., BEVAN, H., QIU, Y., LAGRÈZE, W.A., WYNICK, D., CHURCHILL, A.J., KEHOE, P., HARPER, S.J., BATES, D.O. and DONALDSON, L.F., 2013. VEGF-A165b is an endogenous neuroprotective splice isoform of vascular endothelial growth factor A in vivo and in vitro The American Journal of Pathology. 183(3), 918-929
DRAKE RAR, LEITH JL, ALMAHASNEH F, MARTINDALE J, WILSON AW, LUMB BM and DONALDSON LF, 2016. Periaqueductal grey EP3 receptor activity facilitates spinal nociception in arthritic secondary hypersensitivity Journal of Neuroscience.
My research group concentrates on various aspects of neuronal signalling in chronic pain. We work towards the goal of furthering our understanding of the ways in which the nervous system responds to peripheral injury, to produce protective (useful) and chronic (non-useful) pain. In identifying such mechanisms we aim to contribute to the more effective treatment of pain, by the identification of novel analgesic targets, the development of new, and the better understanding of existing analgesic drugs.
Current projects centre around inflammatory arthritic pain, in models of rheumatoid arthritis, and neuropathic pain, including in traumatic nerve injury and diabetic neuropathy. In a collaborative project with Professor Bridget Lumb (University of Bristol) on arthritic pain, we are studying descending control systems from the brainstem that enhance pain, the central actions of non-steroidal anti-inflammatory drugs (e.g. ketoprofen) on these mechanisms, and spinal cord mechanisms of primary and secondary hyperalgesia. We are also investigating the effects of novel anti-nociceptive agents in these models. Our work on diabetic neuropathy is in collaboration with Professor David Bates, and Dr Richard Hulse, Cancer Biology (University of Nottingham). In this work we are investigating mechanisms of neuronal damage and pain generation in diabetes, and how novel neuroprotective and anti-nociceptive agents might be used to treat diabetic neuropathic pain.