Lucy is a neurophysiologist with expertise in neuronal function in acute and chronic pain, particularly in arthritis but also other painful conditions.
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, neuronal cation-chloride co-transporters and protein kinases . 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, where she has worked on multiple projects ncluding 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 vascular endothelial growth factors in neuroprotection and pain (funded by Diabetes UK and Arthritis Research UK). During this time she also developed a research program in human taste perception in health and disease, with particular focus on taste and depression/anxiety, in collaboration with Jan Melichar. In September 2013, Lucy moved to Life Sciences at the University of Nottingham, where she is now Professor of Sensory Physiology. The main focus of her current work is still in pain, looking at novel analgesic mechanisms for neuropathic and arthritic pain, particularly focussing on alternative RNA splicng. She is a co-founder of a University of Nottingham spin-out company Exonate Ltd, a biopharmaceutical company focussed on the discovery and development of small molecule drugs that modulate alternative mRNA splicing to address diseases of high unmet medical need
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
BEAZLEY-LONG N, MOSS CE, ASHBY WR, BESTALL SM, ALMAHASNEH F, DURRANT AM, BENEST AV, BLACKLEY Z, BALLMER-HOFER K, HIRASHIMA M, HULSE RP, BATES DO and DONALDSON LF, 2018. VEGFR2 promotes central endothelial activation and the spread of pain in inflammatory arthritis. Brain, behavior, and immunity. VED, N., LOBO, M. E. DA VITORIA, BESTALL, S. M., VIDUEIRA, C. L., BEAZLEY-LONG, N., BALLMER-HOFER, K., HIRASHIMA, M., BATES, D. O., DONALDSON, L. F. and HULSE, R. P., 2018. Diabetes-induced microvascular complications at the level of the spinal cord: a contributing factor in diabetic neuropathic pain JOURNAL OF PHYSIOLOGY-LONDON. 596(16), 3675-3693 GREENSPON CM, BATTELL EE, DEVONSHIRE IM, DONALDSON LF, CHAPMAN V and HATHWAY GJ, 2018. Lamina-specific population encoding of cutaneous signals in the spinal dorsal horn using multi-electrode arrays. The Journal of physiology. 597(2), 377-397
BESTALL, SAMUEL M., HULSE, RICHARD P., BLACKLEY, ZOE, SWIFT, MATTHEW, VED, NIKITA, PATON, KENNETH, BEAZLEY-LONG, NICHOLAS, BATES, DAVID O. and DONALDSON, LUCY F., 2018. Sensory neuronal sensitisation occurs through HMGB-1-RAGE and TRPV1 in high-glucose conditions JOURNAL OF CELL SCIENCE. 131(14),
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.
Our current work concentrates on alternative splicing and its contribution to pain and inflammation, and spans arthritis, diabetes and chemotherapy-induced pain.
Previous projects have centred 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 studied 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. Our work on diabetic neuropathy, in collaboration with Professor David Bates, and Dr Richard Hulse, investigated 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.