Troisième conférence mensuelle 2016-2017
Kv1.1 is an axonal potassium channel that is widely expressed in the nervous system, and especially in basket cell terminals of the cerebellar cortex. Dominantly inherited mutations cause Episodic Ataxia type 1. I shall describe our efforts to understand disease mechanisms, new insights into the normal role of Kv1.1 in shaping presynaptic action potentials and neurotransmitter release, and how overexpression of Kv1.1 could be used as gene therapy for focal epilepsy.
Begum R, Bakiri Y, Volynski KE, Kullmann DM. Action potential broadening in a presynaptic channelopathy. Nat Commun. 2016 Jul 6;7:12102. doi: 10.1038/ncomms12102.
Akam T, Kullmann DM. Oscillatory multiplexing of population codes for selective communication in the mammalian brain. Nat Rev Neurosci. 2014 Feb;15(2):111-22. doi: 10.1038/nrn3668.
Ermolyuk YS, Alder FG, Surges R, Pavlov IY, Timofeeva Y, Kullmann DM, Volynski KE.Differential triggering of spontaneous glutamate release by P/Q-, N- and R-type Ca2+ channels. Nat Neurosci. 2013 Dec;16(12):1754-63. doi: 10.1038/nn.3563.
Wykes RC, Heeroma JH, Mantoan L, Zheng K, MacDonald DC, Deisseroth K, Hashemi KS, Walker MC, Schorge S, Kullmann DM. Optogenetic and potassium channel gene therapy in a rodent model of focal neocortical epilepsy. Sci Transl Med. 2012 Nov 21;4(161):161ra152. doi: 10.1126/scitranslmed.3004190.
Scientific focus :
Dimitri Kullmann studied Medicine and Physiology at Oxford and London. Following postdoctoral research in San Francisco he established a laboratory at the UCL Institute of Neurology where his research interests include mechanisms of synaptic transmission and plasticity, neurological channelopathies, experimental gene therapy for epilepsy, and computational properties of simple neural circuits. He also works as a neurologist at the National Hospital, Queen Square, and is the Editor-in-chief of Brain.