Igor Medina

Ihor Medyna (Igor Medina in scientific publications) graduated from the faculty of Biology (chair of Biophysics and Mathematical methods in Biology) in 1982. He received his Ph.D. from Bogomoletz Institute, Kiev and continued training at Cardiology Research Center Moscow, USSR. (1990-93, Dr. P. Bregestovski), at Laboratory of Neurobiology, INSERM U29, Paris, France. (1993-97, Dr. Y. Ben-Ari), and at Children’s Hospital, Harvard Medical School, Boston, USA (1997-2000, Dr. D. E. Clapham). Currently Dr. Medyna holds a permanent senior research position (research director) at the French Medical Research council (INSERM), Paris, France and at Mediterranean Institute of Neurobiology (INMED), Marseille, France. He is a member of the Society for Neuroscience and Guest editor for Frontiers in Cellular Neuroscience.

Ihor Medyna has a broad background in neurobiology and specific expertise in electrophysiology, imaging and cellular biology. He has a long lasting interest in studying the signaling cascades controlling activity of ion channels, channel-coupled receptors and ion transporters. During last decade his research has focused on study of neuronal potassium-chloride co-transporter KCC2, KCC2-dependent chloride homeostasis and GABAergic neurotransmission. As a PI or co-investigator on several funded grants, Dr. Medyna successfully administered projects (staffing, research, and budget), collaborated with other researchers and produced several peer-reviewed publications from each project.

Dr. Ihor Medyna Contribution to Science:

  1. A novel type of stretch-activated channels. During work on my thesis project and first postdoctoral training, I have discovered a new type of stretch activated potassium channels involved in control of resting membrane potential of dividing fish embryos. I showed also importance of phosphorylation for control of ion channels activity. That was one of the first studies in the field describing importance of the phosphorylation to control ion channel activity (1).
  2. Phosphorylation dependent control of G-protein coupled inwardly rectifying channels. This was an important discovery made during work at Harvard University that described a new mechanism controlling activity of the ion channel involved in control of the cardiac rhythm and neuronal activity (2).
  3. NMDA-receptor dependent signaling pathways. A serial of studies directed to identify neuronal activity-dependent signaling cascades involved in control of neuronal plasticity and survival. It includes discovery of i) a new calcium-dependent mechanism controlling NMDAR activity; ii) a new NMDAR-RasGRF1 and SynGAP-MUPP1 protein complexes contributing to signal transfer from the NMDAR and controlling strength of the excitatory transmission; iii) a distinct roles of synaptic and extrasynaptic pools of NMDAR in control of ERK signaling cascade and neuronal survival (3-5).
  4. An important part of my research activity at the INMED was directed on study of the role of the Brain-Derived-Neurotrophic-Factor (BDNF) in maturation and plasticity of GABAergic synapses. This project I was currying in collaboration with team of Dr.Gaiarsa where we performed all molecular biology works and live-cell imaging. We were first to show that activity-dependent dendritic secretion of BDNF can modulate the strength of developing GABAergic synapses. The polarity of the change depends on the form of BDNF secreted and receptor activated: the precursor (proBDNF) through the activation of the p75NTR leads to LTDGABA-A while the mature form (mBDNF) acting on the TrkB receptor leads to LTPGABA-A. We also aimed at determining the pattern of activity and the “synaptic triggers” involved in the activity-dependent secretion of BDNF in the developing brain (6, 7).
  5. KCC2-dependent control of neuronal excitation. A serial of studies directed on analysis of the properties of potassium-chloride co-transporter KCC2, its role in control of the neuronal chloride homeostasis and inhibitory action of GABA. We have found an important role of the KCC2 in control of the expression of GABAA receptors and neuronal resistance to excitotoxic insults. My team also made an important contribution to discovery and characterization of mutations in human KCC2 leading to decrease of transporter activity and associated with idiopathic epilepsy. Finally, in the recent work we have described a novel regulatory pathway WNK1-SPAK-KCC2 contributing to maintenance of the low KCC2 activity and regulating the depolarizing action of GABA in immature neurons (8, 9).

Selected Publications:

  1. P. Bregestovski, I. Medina, E. Goyda, Regulation of potassium conductance in the cellular membrane at early embryogenesis. J. Physiol. Paris. 86, 109–15 (1992).
  2. I. Medina et al., A switch mechanism for G beta gamma activation of I(KACh). J. Biol. Chem. 275, 29709–16 (2000).
  3. I. Medina, N. Filippova, A. Bakhramov, P. Bregestovski, Calcium-induced inactivation of NMDA receptor-channels evolves independently of run-down in cultured rat brain neurones. J. Physiol. 495 ( Pt 2, 411–27 (1996).
  4. G. Krapivinsky et al., The NMDA receptor is coupled to the ERK pathway by a direct interaction between NR2B and RasGRF1. Neuron. 40, 775–84 (2003).
  5. A. Ivanov et al., Opposing role of synaptic and extrasynaptic NMDA receptors in regulation of the extracellular signal-regulated kinases (ERK) activity in cultured rat hippocampal neurons. J. Physiol. 572, 789–98 (2006).
  6. N. Kuczewski et al., Backpropagating action potentials trigger dendritic release of BDNF during spontaneous network activity. J. Neurosci. 28, 7013–23 (2008).
  7. B. Riffault et al., Pro-Brain-Derived Neurotrophic Factor Inhibits GABAergic Neurotransmission by Activating Endocytosis and Repression of GABAA Receptors. J. Neurosci. 34, 13516–13534 (2014).
  8. I. Medina et al., Current view on the functional regulation of the neuronal K+-Cl− cotransporter KCC2. Front. Cell. Neurosci. 8, 1–18 (2014).
  9. P. Friedel et al., WNK1-regulated inhibitory phosphorylation of the KCC2 cotransporter maintains the depolarizing action of GABA in immature neurons. Sci. Signal. 8, 23–26 (2015).

Complete list of Dr. Medyna published works please see here:


Roman Tyzio

Roman Tyzio is a Research Engineer at INMED (INSERM, U901). At Neurochlore, Roman is a researcher responsible for the electrophysiological study of the different models of autism. His research is focused on the role of excitatory and inhibitory receptors and their modulation in developmental and pathological processes. Roman Tyzio obtained his Ph.D. in Physiology from Ivan Franko National University of Lviv (Ukraine). His professional interest is centred on the study of the physiological changes of neuronal functions, and, more particularly, on the development of GABAergic neurotransmission. Dr.  Tyzio has expertise in various electrophysiological and imaging recordings from identified neurons in acute brain slices, slices in culture and transfected fluorescent cells.

Last Publication:

  1. Tyzio R, Nardou R, Ferrari DC, Tsintsadze T, Shahrokhi A, Eftekhari S, Khalilov I, Tsintsadze V, Brouchoud C, Chazal G, Lemonnier E, Lozovaya N, Burnashev N, Ben-Ari Y. Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring. Science. 2014;343(6171):675-9.
  2. Lemonnier E, Robin G, Degrez C, Tyzio R, Grandgeorge M, Ben-Ari Y. Treating Fragile X syndrome with the diuretic bumetanide: a case report. Acta Paediatr. 2013;102(6):e288-90.
  3. Khalilov I, Chazal G, Chudotvorova I, Pellegrino C, Corby S, Ferrand N, Gubkina O, Nardou R, Tyzio R, Yamamoto S, Jentsch TJ, H?bner CA, Gaiarsa JL, Ben-Ari Y, Medina I. Enhanced Synaptic Activity and Epileptiform Events in the Embryonic KCC2 Deficient Hippocampus. Front Cell Neurosci. 2011;5:23.
  4. Ben-Ari Y, Tyzio R, Nehlig A. Excitatory action of GABA on immature neurons is not due to absence of ketone bodies metabolites or other energy substrates. Epilepsia. 2011;52(9):1544-58.
  5. Tyzio R, Allene C, Nardou R, Picardo MA, Yamamoto S, Sivakumaran S, Caiati MD, Rheims S, Minlebaev M, Milh M, Ferr? P, Khazipov R, Romette JL, Lorquin J, Cossart R, Khalilov I, Nehlig A, Cherubini E, Ben-Ari Y. Depolarizing actions of GABA in immature neurons depend neither on ketone bodies nor on pyruvate. J Neurosci. 2011;31(1):34-45.


Victor Chaban

Dr. Chaban received his Ph.D. from Bogomoletz Institute, Kiev and continued his training at Babraham Institute, Cambridge, U.K. Prior to coming to UCLA he worked at Nencki Institute in Warsaw. Dr. Chaban completed his post-doctoral training in Neuroscience at the Department of Medicine at UCLA and graduate training in Clinical Research at Charles Drew University of Medicine and Science. Currently Dr. Chaban is an Associate Professor of Medicine. He received Wood-Whellan Award from International Union of Biochemistry and Molecular Biology and Fellowships from International Science Foundation, European Science Foundation and UNESCO. He also received 2008 President’s Award for Excellence in Service to Charles Drew University and 2009 Life Sciences Institute Emerging Scientist Award. Dr. Chaban’s area of expertise includes hormonal modulation of pain transmission at the level of primary afferent neurons and non-genomic effects of sex steroids.

Last Publication:

  1. Chaban VV. Visceral Pain: Basic Research Concepts and Therapeutic Interventions. Int J Res Nurs. 2015;6(2):27-28.
  2. Chaban VV, Cho T, Reid CB, Norris KC. Physically disconnected non-diffusible cell-to-cell communication between neuroblastoma SH-SY5Y and DRG primary sensory neurons. Am J Transl Res. 2013;5(1):69-79.
  3. Cho T, Chaban VV. Expression of P2X3 and TRPV1 receptors in primary sensory neurons from estrogen receptors-α and estrogen receptor-β knockout mice. Neuroreport. 2012;23(9):530-4.
  4. Chaban VV, Cho T Reid CB, Norris KC Physically disconnected non-diffusible cell-to-cell communication between neuroblastoma SH-SY5Y and DRG primary sensory neurons American journal of translational research, 2013; 5(1): 69-79.
  5. Chaban VV.Peripheral sensitization of sensory neurons.Ethn Dis. 2010;20(1 Suppl 1):S1-3-6.


No alumnus found.