emmanuel bourinet
  • E-mail :[email]
  • Phone : +33 4 34 35 92 48
  • Location : Montpellier, France
Last update 2019-09-20 15:07:31.516

emmanuel bourinet PhD in physiology

Course and current status

Positions and Employment

2005-present     Group leader / PI – Institute of Functional Genomics Montpellier France

2005-2015            Directeur de recherche  1ère classe (DR2)  CNRS

2005-2015            Directeur de recherche  2ème classe (DR2)  CNRS

2002-2004            Chargé de recherche  (CR1) CNRS, IGH Montpellier France

1996-2002            Chargé de recherche  (CR2) CNRS, CRBM Montpellier France

1993-1995            Postdoctoral Fellow, Terrence Snutch lab, Biotechnology laboratory, The University of British Columbia, Vancouver Canada

1990-1993           Thesis student, Montpellier University

Scientific summary

The goal of the research performed in my team at the institute de Génomique Fonctionnelle in Montpellier, is to investigate the role of T-type calcium channels in the development of chronic pain and in particular in neuropathic pain conditions. Specifically, we tackle this problem combining the use of mouse models, in vitro electrophysiology, molecular biology and biochemistry to determine the molecular mechanism by which T-type currents support changes in electrical excitability of dorsal root neurons that underlie neuropathic pain responses. I authored 76 papers and 2 patents so far, all related to the field of ion channels and mostly in the context of pain pathophysiology.

I have a background in physiology with specific training in key research areas of relevance for this application.  I have a long standing interest in the molecular properties and regulations of voltage gated calcium channels since my thesis performed with Dr Nargeot in Montpellier in the early 90ies and then during my postdoctoral training at the University of Birtish Columbia in Vancouver (Canada) working with Dr Terry Snutch. My key findings at that time are the identification of the molecular nature of P- and Q-type calcium channels encoded by 2 splice variants of the Cav2.1 gene, and the identification of the G beta gamma proteins as the regulators of voltage gated Ca channels downstream of GPCR activation. After getting a position in Montpellier I developed a research axis on the understanding of T-type calcium channel role in sensory neuron.  We demonstrated that T-type ion channels can be effectively knocked down in sensory neurons by intrathecal injections on CaV3.2 antisenses. This effect leads to a potent analgesic effects regarding both somatic and visceral pain perception. We showed that CaV3.2 T-type channel sensitization play an important role in the pathophysiology of sensory neuron hyper-excitability. To provide insight into the channel dynamics, we were the first to engineer surface epitope tagged calcium channel subunits including CaV3.2. These tools were largely distributed and used in laboratories in the field. Currently, our project focus on the use of a genetically modified mouse model that we created with a GFP variant inserted at the CaV3.2 surface. This model is tailored to study CaV3.2 dynamics in the context of sensory neuron pathophysiology. The presentation will focus on the use of this mouse model in my group to decipher the impact of the Cav3.2 calcium channel in the development of chronic pain.

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