Dr Richard Hulse is a Lecturer in neuroscience and pharmacology, investigating how the sensory nervous system regulates pain perception in health and disease. He is module lead for MSc research projects (BIOL 40111)
During his PhD in the Pain Research Group at the University of Bristol, Dr Hulse developed an interest in sensory neurophysiology, investigating the role that sensory primary afferents have in neuropathic pain. He acquired skills in electrophysiological and behavioural assays to understand how the neuropeptide galanin modulates this system.
In a subsequent postdoctoral position at the University of Bristol Dr Hulse extended his pain research portfolio and skillset by investigating the role of the vascular endothelial growth factor-A (VEGF) family in nociception. This encompassed research into peripheral and central neuronal sensory processing of pain signals as well as vascular biology to examine how VEGF and alternative splicing can alter pain processing; primarily using pharmacological intervention; current and novel agents.
In 2013 he was appointed as Senior Research Fellow at Nottingham University to focus on cancer related pain in the Division of Cancer and Stem Cell Sciences. Having spoken directly to diabetic and cancer patients who suffer from pain, he is directly aware of how this can impact upon quality of life and forms the basis for many of the research questions he wishes to answer. Understanding the neurophysiology responsible for controlling pain is crucial if we are to understand what goes wrong in chronic pain sufferers. He is targeting clinical problems currently underrepresented by basic research in the hope that we may develop new analgesics for chronic pain sufferers.
The research questions he wishes to answer are those based upon understanding the neurophysiology responsible for controlling pain and in particular highlighting those instances where these neuronal systems are altered leading to chronic pain. Chronic pain is highly debilitating due to elevated levels of pain and persistent pain, which arise through a number of varying causes with those areas investigated including diabetes, chemotherapy, tumour induced, arthritis and physical trauma.
Further work is being undertaken to understand how persistent pain arises in cancer patients and how cancer therapies (adult and children) impact upon the nervous system leading to long lasting aberrant sensations.
Current research areas include:
Diabetic neuropathic pain affects as many as 50% of patients suffering from sensory complications (burning pain, pins and needles). To date the efficacy and longevity of many current pain-killing drugs is poor. It is widely known that the plasticity of the sensory nervous system strongly underpins neuropathic pain through changes in the organisation, morphology and excitability of sensory neurons resulting in the summation and amplification of sensory signals. Our work to date highlights that in diabetics there is a significant alteration in how the sensory neurons modulates sensory information due to changes neurovascular coupling. We wish to establish how hyperglycaemia drives sensory neuron excitability to develop new treatment approaches for diabetic neuropathic pain.
Chemotherapy and immunotherapy induced sensory neuropathy affects many cancer patients (~70%), both adults and children. The impact of disease or physical impact on neuronal systems leads to an array of sensory neuronal alterations; principally resulting in neuronal cell death and neural degeneration highlighted by nerve regression and neuronal apoptosis. These events affect neuronal signalling and neurotransmission, ultimately leading to the manifestation of pain. Unfortunately sensory neurons have a poor recovery/regeneration rate. This is likely to be attributable due to the loss of necessary growth/support factors such as VEGF-A. This is as a result of reduced transcriptional or translational processing indicating compromised repair processes. We are currently defining how chemotherapy can damage the sensory nervous system and activate the immune system but also establishing how this activates the sensory neurons to cause pain. By targeting these mechanisms we believe we can understand chemotherapy induced sensory neurodegeneration and pain, allowing us to effectively treat pain in the future.
We utilise cell culture and rodent based assays inclusive of histology, behavioural assessment and electrophysiological studies incorporating biochemical techniques
Sponsors and collaborators
- European Foundation for the Study of Diabetes
- The Rosetrees Trust
HATHWAY, G.J., MURPHY, E., LLOYD, J., GREENSPON, C. and HULSE, R.P., 2017. Cancer chemotherapy in early life significantly alters the maturation of pain processing.Neuroscience. ISSN 0306-4522
AUSTIN, M., ELLIOTT, L., NICOLAOU, N., GRABOWSKA, A. and HULSE, R.P., 2017. Breast cancer induced nociceptor aberrant growth and collateral sensory axonal branching. Oncotarget, 8 (44), pp. 76606-76621. ISSN 1949-2553
HULSE, R.P., 2016. Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia. European Journal of Pain, 20 (4), pp. 615-625. ISSN 1090-3801
HULSE, R.P., BEAZLEY-LONG, N., VED, N., BESTALL, S.M., RIAZ, H., SINGHAL, P., BALLMER HOFER, K., HARPER, S.J., BATES, D.O. and DONALDSON, L.F., 2015. Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration. Clinical Science, 129 (8), pp. 741-756. ISSN 0143-5221See all of Richard Hulse's publications...