!Curriculum Vitae
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Dimitri M Kullmann MA DPhil FRCP FFICM FMedSci \\
Professor of Neurology, UCL Institute of Neurology\\
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Education\\
Oxford University: \\
BA 1979 Physiological Sciences\\
DPhil 1984\\
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London University:\\
MB BS 1986 Medicine\\
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Editorships\\
Brain: Editor-in-Chief (2014 – present) \\
Neuron: Editorial Board (1997 – present)\\
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Current Research Funding\\
2015 – 2018: MRC "Activity-dependent regulation of synaptic strength and cellular mechanisms of migraine" (KE Volynski, I Pavlov, DMK) £727,994\\
2015 – 2018: MRC "Periodic paralysis: from molecules to mice" (R Mannikko, DMK, MG Hanna, S Schorge) £467,547\\
2015 – 2020:  Wellcome Trust "Synaptopathies: genetics, biophysical and circuit mechanisms of paroxysmal neurological disorders" (DMK, K Volynski, S Schorge, MG Hanna, H Houlden, JE Rothman, J Jepson, S Sisodiya, PJ Goadsby) £4m\\
2014 – 2019: MRC "Gene therapy for refractory epilepsy" (DMK, S Schorge, MC Walker) £3.1m \\
2011 – 2018: Wellcome Trust Senior Investigator "Synaptic neurology" £2.3m\\
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Current Sponsorship\\
Wellcome Trust Clinical Postdoctoral Fellowship for S Crisp; Epilepsy Research UK Fellowship for R Wykes; Marie-Curie Fellowships for G Lignani, A Lieb and H Martin.\\
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Research\\
1979 – 1983, 1987 – 1989, Oxford: DPhil & postdoctoral research with Julian Jack: Feedback gain in the segmental spinal motor circuitry in a decerebrate vertebrate preparation; quantal analysis to unitary postsynaptic signals in the spinal cord. This work revealed presynaptic sites of action of the GABAB receptor agonist baclofen and anaesthetic agents.\\
1990 – 1992, UCSF: Postdoctoral work with Roger Nicoll. I showed that long-term potentiation (LTP) of synaptic transmission is associated with increases in both quantal content and quantal amplitude, and described a form of non-associative plasticity.\\
1992 – 1997, Institute of Neurology: Discovery of ‘silent synapses’ and spillover-mediated heterosynaptic actions of glutamate on NMDA and metabotropic glutamate receptors. \\
1997 – 2007, UCL: Extra- and heterosynaptic signaling mediated by glutamate and GABA. Discovery of tonic inhibition in interneurons and two forms of LTP in interneurons. Biophysical mechanisms of channelopathies.\\
2007 – present, UCL: Quantitative analysis of calcium-exocytosis coupling in small excitatory boutons; gene therapy for experimental epilepsy; mechanisms of inherited and autoimmune channelopathies; dynamical analysis of network oscillations. \\
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Clinical work: neurology, synaptopathies and neurological intensive care.\\ \\