Norbert Weiss
  • E-mail :[email]
  • Phone : 1 403 220 6597
  • Location : Prague, the Czech Republic

Scientific topics

Keywords

Last update 2014-09-17 20:54:10.948

Norbert Weiss PhD Neurosciences - Electrophysiology - Ion channels

Course and current status

CURRENT STATUS  

  • Postdoctoral fellow in the laboratory of Dr. Gerald W. Zamponi, Hotchkiss Brain Institute, department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.

 

EDUCATION

  • 2001: BS degree in Cellular Biology and Physiology, University Joseph Fourier, Grenoble, France
  • 2003: MS degree in Cellular and Molecular biology, University Joseph Fourier, Grenoble, France
  • 2006: PhD in Neurosciences-Neurobiology, University Joseph Fourier, Grenoble, France

 

RESEARCH EXPERIENCE

  • 2000 – 2001: Summer student, Laboratory of Physiology, Grenoble Hospital, Grenoble, France. (supervisor Pr. Bruno Bonaz)
  • 2002 – 2003: Master student, Laboratory of ion Channels, Functions and Pathologies (INSERM U607), Grenoble, France. (supervisor Dr. Michel De Waard)
  • 2003 – 2006: PhD student, Laboratory of ion Channels, Functions and Pathologies (INSERM U607), Grenoble, France. (supervisor Dr. Michel De Waard)
  • 2007 – 2008: Postdoctoral fellow, Laboratory of Integrative Cellular and Molecular Physiology (CNRS UMR5123), Villeurbanne, France. Funded by the National Agency of Research - Rare diseases grant. (supervisors Drs. Vincent Jacquemond and Bruno Allard)
  • 2008 – 2009: Postdoctoral fellow, Biochip laboratory (CEA Grenoble), Grenoble, France. Funded by a CEA fellowship.
  • 2009 – 2010: Postdoctoral fellow, Grenoble Institute of Neurosciences (INSERM U836), Grenoble, France. Funded by the National Agency of Research.
  • 2011 – present: Postdoctoral fellow, Hotchkiss Brain Institute, department of Physiology and Pharmacology, University of Calgary, Calgary, Canada. Funded by Hotchkiss Brain Institute and Alberta Innovates-Health Solutions fellowships.

Scientific summary

My research focuses on voltage-gated calcium channels (VGCCs). Calcium influx via VGCCs plays essential roles in a variety of physiological processes including synaptic transmission, synaptic plasticity or gene transcription/translation etc. Dysfunction of VGCCs is linked to numerous diseases (called channelopathies) including epilepsy, migraine or pain. I am investigating the cellular and molecular contributions of VGCCs in physiological functions and pathphysiological processes with the ultimately goal that it could lead to a better understanding and development of pharmacological tools to treat calcium channelopathies.

PUBLICATIONS  

  1. Weiss N, Zamponi GW (in press) Regulation of voltage-gated calcium channels by synaptic proteins. Advances in Experimental Medicine and Biology - Springer.
  2.  Weiss N, Sandoval A, Kyonaka S, Felix R, Mori S, De Waard M (2011) Rim1 modulates direct G-protein regulation of Cav2.2 channels. Pflügers Arch – Eur J Physiol 461:447-59.
  3. Weiss N (2011) Control of depolarization-evoked presynaptic neurotransmitter release by Cav2.1 channel: Old story, new insights. Channels (Austin) 4:431-3.
  4. Taïwe GS, Ngo Bum E, Dimo T, Talla E, Weiss N, Dawe A, Moto FCO, Sidiki N, Dzeufiet PD, De Waard M (2011) Antidepressant, myorelaxant and anti-anxiety-like effects of Nauclea latifolia Smith (Rubiaceae) roots extract in murine models. Pharma Biol 49:15-25.
  5. Weiss N, Legrand C, Pouvreau S, Bichraoui H, Allard B, Zamponi GW, De Waard M, Jacquemond V (2010) In vivo expression of the G-protein b1g2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling. J Physiol (London) 588:2945-60.
  6. Weiss N, Andrianjafiniony T, Dupre-Aucouturier S, Pouvreau S, Desplanches D, Jacquemond V (2010) Altered myoplasmic Ca2+ handling in rat fast-twitch skeletal muscle fibres during disuse atrophy. Pflügers Arch – Eur J Physiol 459:631-44.
  7. Weiss N (2009) Regulation of N-type calcium channels by G-proteins: multiple pathways to control calcium entry into neurons. Channels (Austin) 3:219-220.
  8. Berbey C, Weiss N, Legrand C, Allard B (2009) Transient receptor potential canonical type 1 (TRPC1) operates as a sarcoplasmic reticulum calcium leak channel in skeletal muscle. J Biol Chem 284:36387-94.
  9. Al-Qusairi L, Weiss N, Toussaint A, Berbey C, Messaddeq N, Kretz C, Sanoudou D, Beggs A, Allard B, Mandel JL, Laporte J, Jacquemond V, Buj-Bello A (2009) T-tubule disorganization and defective excitation-contraction coupling in muscle fibers lacking myotubularin lipid phosphatase. Proc Natl Acad Sci 106:18764-68.
  10. Ram N, Weiss N, Texier-Nogues I, Aroui S, Pirrolet F, Ronjat M, Darbon H, Jacquemond V, De Waard M (2008) Design of a disulfide-less, pharmacologically-inert and chemically-competent analogue of maurocalcine for the efficient transport of impermeable compounds into cells. J Biol Chem 283: 27048-56.
  11. Weiss N, Sandoval A, Felix R, Van den Maagdenberg A, De Waard M (2008) The S218L familial hemiplegic migraine mutation promotes deinhibition of Cav2.1 calcium channels during G-protein regulation. Pflügers Arch – Eur J Physiol 457: 315-26.
  12. Weiss N, Legrand C, Couchoux H, Berthier C, Allard B, Jacquemond V (2008) Expression of the dystrophy-associated caveolin-3P104L mutant in adult mouse skeletal muscle specifically alters the Ca2+ conducting function of the dihydropyridine receptor. Pflügers Arch – Eur J Physiol 457: 361-75.
  13. Weiss N (2008) The N-type voltage-gated calcium channel: when a neuron reads a map? J Neurosci 28:5621-5622.
  14. Weiss N, Ivanova E (2008) Does the voltage-gated calcium a2d-1 subunit play a dual function in skeletal muscle? J Physiol (London) 586: 2035-2037.
  15. Weiss N (2007) Alternative splicing of the Cav2.2 subunit: a change in N-type calcium channel activity for which purpose? J Physiol (London) 580: 361-362.
  16. Weiss N, Tournier-Lasserve E, De Waard M (2007) Role of P/Q calcium channel in familial hemiplegic migraine. Med Sci (Paris) 23: 53-63.
  17. Weiss N, Tadmouri A, Mikati M, Ronjat M, De Waard M (2007) Importance of voltage-dependent inactivation in N-type calcium channel regulation by G-proteins. Pflügers Arch – Eur J Physiol 454: 115-129.
  18. Weiss N, De Waard M (2007) Introducing an alternative biophysical method to analyse direct G protein regulation of voltage-dependent calcium channels. J Neurosci Methods 160: 26-36.
  19. Weiss N, Arnoult C, Feltz A, De Waard M (2006) Contribution of the kinetics of G proteins dissociation to the characteristic modifications of N-type calcium channel activity. Neurosci Res 56: 332-343.
  20. Weiss N (2006) The calcium channel b4a subunit: a scaffolding protein between voltage-gated calcium channel and presynaptic vesicle-release machinery. J Neurosci 26: 6117-6118.
  21. Weiss N, De Waard M (2006) Voltage-dependent calcium channels at the heart of pain perception. Med Sci (Paris) 22: 396-404.
  22. De Waard M, Hering J, Weiss N, Feltz A (2005) How do G proteins directly control neuronal Ca2+ channel function? Trends Pharmacol Sci 26: 427-436.
  23. Sandoz G, Lopez-Gonzalez I, Stamboulian S, Weiss N, Arnoult C, De Waard M (2004) Repositioning of charged I-II loop amino acid residues within the electric field by b subunit as a novel working hypothesis for the control of fast P/Q calcim channel inactivation. Eur J Neurosci 19: 1759-1772.
  24. Sandoz G, Lopez-Gonzalez I, Bichet D, Altafaj X, Weiss N, Ronjat M, Dupuis A, De Waard M (2004) Cavb-subunit displacement is a key step to induce the reluctant state of P/Q calcium channels by direct G protein regulation. Proc Natl Acad Sci 1001: 6267-6272.
  25. Cuchillo-Ibanez I, Aldea M, Brocard J, Albillos A, Weiss N, Garcia AG, De Waard M (2003) Inhibition of voltage-gated calcium channels by sequestration of b subunits. Biochem Biophys Res Comm 311: 1000-1007.

 

BOOK CHAPTER

  • Calcium signaling. Springer - Advances in Experimental Medicine and Biology. [url]http://calciumsignaling.islets.se[\url]  
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