Professor Janusz Lipski

Biography

Professional and academic experience

Current appointment (from 1987): Chair in Neurophysiology, Deptartment of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand

2007-present Foreign Member of the Polish Academy of Science (PAU, Krakow)
1987-present Professor of Neurophysiology, The University of Auckland, New Zealand
1984-87 Senior Research Fellow, Experimental Neurology Unit, The John Curtin School of Medical Research, ANU, Canberra, Australia
1980-84 Associate Professor (Dozent Dr.), Dept. of Physiology, Univ. of Warsaw, Poland
1977-79 UNESCO / IBRO Fellow, Dept. of Neurophysiology, Univ. of Goteborg, Sweden
1975-77 Lecturer and Senior Lecturer, Dept. of Physiology, Univ. of Warsaw, Poland

 

Research | Current

Research interests

 

Summary of research programme

Molecular Neurophysiology website 

The aim of our research is to characterise the cellular and molecular mechanisms of neuronal damage occurring acutely during stroke, or chronically in such neurological disorders as Parkinson's disease or ALS. Currently, we are focusing on pathophysiology of two neuronal groups: (i) CA1 pyramidal neurons in the hippocampus, which is one of the groups of cells in the brain most vulnerable to ischemia; and (ii) dopaminergic neurons of the Substantia Nigra which degenerate in Parkinson's disease. In this latter group, we are studying the effects of neurotoxins (eg. 6-hydroxydopamine, rotenone) and of L-DOPA (Levodopa). One of the main objectives is to test the hypothesis that both the acute and chronic neuronal damage is associated with activation of a novel group of calcium and other cation-permeable cell membrane proteins known as TRP channels, which open as a result of metabolic and oxidative stress.

This hypothesis is tested using in vitro models (in acute brain slices and organotypic slice cultures). Finding the role of TRP and other (eg. K+ATP) channels in controlling cation fluxes in vulnerable brain cells should lead to new pharmacological treatments not only for stroke and Parkinson's disease, but also of other neurodegenerative disorders associated with excitotoxicity, calcium overload and oxidative stress.

In research focusing on the mechanisms of damage of CA1 hippocampal neurons and dopaminergic neurons in the Substantia Nigra during ischemia and reperfusion we are looking at the potential neuroprotective role of novel, 'mitochondrial-targeted' antioxidants.  We are detecting changes in ROS production and monitoring other indices of mitochondrial function (eg. mitochondrial membrane potential) as well as the occurrence of ‘Hypoxic Spreading Depression’. Another area of our interest includes the function of glutamate transporters (in particular GLT-1) and the ways of enhancing the action of these transporters to reduce excitotoxic cell death.

Major experimental techniques include electrophysiology (whole-cell patch-clamp and intracellular recordings with sharp microelectrodes), calcium imaging (using fura-2), measurement of cell swelling (tissue impedance and intrinsic optical properties), ROS production (using dihydroethidine), time course of stress-induced cell death process (dynamic imaging with propidium iodide), single cell labelling with fluorescent and other markers, immunocytochemistry/Western blots, and pharmacological modulation of specific membrane receptors. Analysis of gene expression is conducted with RT-PCR. 

Selected publications and creative works (Research Outputs)

  • Karunasinghe, R., Grey, A., Telang, R., Vlajkovic, S., & Lipski, J. (2017). Differential spread of anoxic depolarization contributes to the pattern of neuronal injury after oxygen and glucose deprivation (OGD) in the Substantia Nigra in rat brain slices. Neuroscience, 340, 359-372. 10.1016/j.neuroscience.2016.10.067
    URL: http://hdl.handle.net/2292/32713
    Other University of Auckland co-authors: Gus Grey, Srdjan Vlajkovic, Rashika Karunasinghe
  • Yee, A. G., Freestone, P. S., Bai, J.-Z., & Lipski, J. (2017). Paradoxical lower sensitivity of Locus Coeruleus than Substantia Nigra pars compacta neurons to acute actions of rotenone. Experimental Neurology, 287 (1), 34-43. 10.1016/j.expneurol.2016.10.010
    URL: http://hdl.handle.net/2292/31694
    Other University of Auckland co-authors: Peter Freestone
  • Freestone, P. S., Wu, X. H., de Guzman, G., & Lipski, J. (2015). Excitatory drive from the Subthalamic nucleus attenuates GABAergic transmission in the Substantia Nigra pars compacta via endocannabinoids. European Journal of Pharmacology, 767, 144-151. 10.1016/j.ejphar.2015.09.050
    URL: http://hdl.handle.net/2292/33071
    Other University of Auckland co-authors: Peter Freestone
  • Burrell, M. H., Atcherley, C. W., Heien, M. L., & Lipski, J. (2015). A novel electrochemical approach for prolonged measurement of absolute levels of extracellular dopamine in brain slices. ACS Chemical Neuroscience, 6 (11), 1802-1812. 10.1021/acschemneuro.5b00120
    URL: http://hdl.handle.net/2292/33075
  • Yee, A. G., Lee, S.-M., Hunter, M. R., Glass, M., Freestone, P. S., & Lipski, J. (2014). Effects of the Parkinsonian toxin MPP+ on electrophysiological properties of nigral dopaminergic neurons. Neurotoxicology, 45, 1-11. 10.1016/j.neuro.2014.08.009
    Other University of Auckland co-authors: Michelle Glass, Peter Freestone
  • Freestone, P. S., Guatteo, E., Piscitelli, F., di Marzo, V., Lipski, J., & Mercuri, N. B. (2014). Glutamate spillover drives endocannabinoid production and inhibits GABAergic transmission in the Substantia Nigra pars compacta. Neuropharmacology, 79, 467-475. 10.1016/j.neuropharm.2013.12.007
    Other University of Auckland co-authors: Peter Freestone
  • Bai, J.-Z., & Lipski, J. (2014). Involvement of TRPV4 channels in Aβ(40)-induced hippocampal cell death and astrocytic Ca(2+) signalling. Neurotoxicology, 41, 64-72. 10.1016/j.neuro.2014.01.001
  • Guatteo, E., Yee, A., McKearney, J., Cucchiaroni, M. L., Armogida, M., Berretta, N., ... Lipski, J. (2013). Dual effects of l-DOPA on nigral dopaminergic neurons. Experimental Neurology, 247, 582-594. 10.1016/j.expneurol.2013.02.009