Dr Mark Baker
Non-clinical lecturer in Neuroscience
Centre: Neuroscience and Trauma
Email: email@example.comTelephone: 020 7882 2287
Mark Baker completed an honours degree in Physiology at Leeds University in 1981. Following his PhD studies on the hippocampus in St Andrews, he spent two post-docs with Hugh Bostock FRS at the Institute of Neurology studying the function and pharmacology of axonal ion channels, and he assisted Hugh in devising the methodology for ‘threshold-electrotonus’ recording, now used clinically to assess peripheral nerve function. Mark gained experience of pharmacology in industry at Pfizer in the 1980s, and then in the lab of J. Murdoch Ritchie FRS in the department of Pharmacology at Yale. While in the USA, Mark made a detailed characterization of the potassium channels expressed in Schwann cells, using polypeptide neurotoxins. Mark was a member of John Wood's molecular nociception group at UCL from 2000 to 2005, and he studied the effects of Na+ channel gene knock-out or mutation on damage sensing neurones, using patch-clamp techniques. Mark has made contributions to understanding the roles played by distinct Na+ channel sub-types in generating neuropathic and inflammatory pain. He was appointed non-clinical lecturer in Neuroscience in 2005.
Lead practical class demonstrator for Brain and Behaviour module, GEP and MBBS
MBBS Lecturer Year 1, PBL facilitator MBBS year 1 and 2
BSc Neuroscience (Intercalated), Lecturer and lab project supervisor
BSc in Experimental Pathology (Intercalated), Lecturer
MSc Neuroscience and Translational Medicine, Lecturer and lab project supervisor
Topics for PhD supervision
Molecular and cellular neuroscience: ion channels and the control of nerve excitability and sensory signalling
Mark’s recent research interests have included defining the role of an arachidonic acid metabolite, 20-HETE, in the gating and modulation of TRPV1, in collaboration with Amrita Ahluwalia (Wellcome Trust supported). He has devised a method of non-invasive VEP recording to assess visual system integrity in animal models of MS with David Baker and Gavin Giovannoni (NC3R supported). Most recently, Mark has investigated the functional impact of electroneutral Na+ transport in normal and diseased central axons (MS society innovation award) and in a new collaboration with John Viles he is investigating mechanisms of amyloid-b cellular toxicity (QMUL Life Sciences Initiative and BBSRC supported).
Okuse K, Malik-Hall M, Baker MD, Poon W-YL, Kong H, Chao MV and Wood JN (2002). Annexin II light chain regulates sensory neuron specific sodium channel expression. Nature 417 : 653-656.
Fertleman CR, Baker MD, Parker KA, Moffatt S, Elmslie FV, Abrahamsen B, Ostman J, Klugbauer N, Wood JN, Gardiner RM and Rees M (2006). SCN9A mutations in Paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron 52 : 767-774.
Östman JAR, Nassar MA, Wood JN and Baker MD (2008) GTP up-regulated persistent Na+ current and enhanced nociceptor excitability require NaV1.9 Journal of Physiology 586: 1077-1088
Wen H, Östman J, Bubb KJ, Panayiotou C, Priestley JV, Baker MD, Ahluwalia A (2012) 20-hydroxyeicosatetraenoic acid (20-HETE) is a novel activator of TRPV1. Journal of Biological Chemistry 287:13868-13876.
Coates TA, Woolnough O, Masters JM, Asadova G, Chandrakumar C, Baker MD. Acute temperature sensitivity in optic nerve explained by an electrogenic membrane potential (2015) Pflugers Arch Eur J Physiol 467, 2337-2349. DOI 10.1007/s00424-015-1696-2
View all Mark Baker's Research Publications at: http://www.researchpublications.qmul.ac.uk