Following his graduation as an MD at University Medical School Debrecen, Hungary in 1982, Dr Nagy started to work as a neuroscientist. He obtained his PhD at the Hungarian Academy of Sciences in 1996. Recently he has also obtained the title of Dr. Habil.
Dr Nagy has been working on the mechanisms involved in peripheral and spinal neuronal processing for 30 years . He has been particularly interested in the neurochemistry, physiology and pharmacology of nociceptive processing.
Dr Nagy has been working at Imperial College London since 1998, where he is one of the leading basic pain scientists. His pioneering work on heat transduction mechanisms and interactions between the endovanilloid and endocannabinoid systems has significantly contributed to the knowledge, which underlies the recent development of novel pharmacological approaches for pain control.
Dr Nagy uses a broad repertoire of techniques including molecular, biochemical, electrophysiological, pharmacological, morphological and behavioural approaches. Dr Nagy is the principal author of many highly-cited, seminal publications in peer-reviewed journals and books. He is a regularly invited speaker, key-note presenter and session organiser at various international conferences.
As a principal investigator, Dr Nagy leads the work of a group of undergraduate and postgraduate students, as well as postdoctoral scientists. He has extensive collaboration with several academic and industrial scientists both within the UK and overseas.
Current actiities in Dr Nagy's laboratory:
Dr Nagy has been working on transduction mechanisms in primary sensory neurons for more than 10 years. Currently Dr Nagy and his co-workers are interested in the mechanisms in mechanotransduction, particulalry in those which are involved the development of inflmmatory visceral hyper-reflexia.
Endocannabinoid and endocannabinoid system:
In order to utalise the potential of the endovanilloid and endocannabinoid systems for pain control, Dr Nagy and his co-workers study the role of various enocannabinoid/endovanoilloid molecules on the rugulation of nociceptive processing in primary sensory neurosn and the spinal cord. In this work they pay particular attention on the role of anandamide, by studying the actions and metabolism of this molecule.
Nociceptive mechanisms in burn injury:
In order to increase our understanding of the peripheral signalling mechanisms involved in the development of burn injury-associated pain, and to identify new target(s) for the development of novel analgesics for controlling burn injury-associated pain, Dr Nagy' laboratory is engaged in studies on signalling between agents accumulating in burnt tissues and sensory nerve endings innervating burnt tissues. In this work, Dr Nagy and his co-workers generate metabolomic and gene expression tissue databases of various degrees of burn injury (volunteer, burn-injured patients and rats) and rat primary sensory neurons, respectively. Analysing these databases will reveal putative targets for new therapeutic approaches to control pain in burn-injured patients.
Dr Nagy has recently started to study mechanisms involved in the development of tension headache and migraine. He and his co-workers are particulalry interested in the role of hypothalamus, and mechanotransduction in trigeminal ganglionic neurons in the development of headache.
et al., 2021, Histone post-translational modification as potential therapeutic targets for pain management, Trends in Pharmacological Sciences, ISSN:0165-6147
et al., 2021, (-)-Englerin-A has analgesic and anti-inflammatory effects independent of TRPC4 and 5, International Journal of Molecular Sciences, Vol:22, ISSN:1422-0067
et al., 2021, Spinal excitatory dynorphinergic interneurons contribute to burn injury-induced nociception mediated by phosphorylated histone 3 at serine 10 in rodents, International Journal of Molecular Sciences, Vol:22, ISSN:1422-0067, Pages:1-28
et al., 2021, TRPV1 feed-forward sensitisation depends on COX2 upregulation in primary sensory neurons, Scientific Reports, Vol:11, ISSN:2045-2322
et al., 2021, Imidazoline ligand BU224 reverses cognitive deficits, reduces microgliosis and enhances synaptic connectivity in a mouse model of Alzheimer’s disease, British Journal of Pharmacology, Vol:178, ISSN:0007-1188, Pages:654-671