Giovanni Marsicano
  • E-mail :[email]
  • Phone : +33 5 57 57 37 56
  • Location : Bordeaux, France
Last update 2013-12-20 16:09:29.68

Giovanni Marsicano PhD in Neurobiology and Degree in Veterinary Medicine

Course and current status

Current status: Research Director at Inserm

Group leader of the Team “Endocannabinoids and Neuroadaptation”, INSERM U862 NeuroCentre Magendie, Bordeaux (France)


1981-1986: High School Diploma, Liceo Classico “F. Delpino”, Chiavari (Genova, Italy)

1986-1992: Degree in Veterinary Medicine (marks 110/110 cum laude), University of Parma (Italy);

1997-2001: Ph.D degree in Neurobiology, Open University Milton Keynes (UK)

 Work experience

1993-1995 : Researcher in the laboratory of Dr Cesare Galli at the Laboratory of Technology of Reproduction in Cremona (Italy), in the EU Project“Stem Cells in farm animals” (IV Framework).

1995-1997: Researcher in the laboratory of Dr Mara Rossini, at the Molecular Biology Department of Chiron SpA Research Center in Siena (Italy).

1997-2001: Ph.D. student in the group of Dr Beat Lutz, at the Max-Planck Institute of Psychiatry in Munich, Germany.

2001-2004: Post-Doc fellow in the group of Dr Beat Lutz, at the Max-Planck Institute of Psychiatry in Munich, Germany.

2005-2006: Teaching in Physiological Chemistry (in anticipation of a position as Junior Professor at the Johannes Gutenberg-University Mainz, Germany

2006: AVENIR  position at INSERM U862 NeuroCentre Magendie in Bordeaux (France).

Group leader of the Team “Endocannabinoids and Neuroadaptation”.

2007-2012 : CR1 (Chargè de Recherche) Permanent senior scientist position at Inserm

From 2012: DR2 (Directeur de Recherche, first ranked at National French Concours) position at Inserm

Main Prices and Honors

2013: Grand Prix Robert Debré for Fundamental Research in Biomedicine

2010: Award of European Research Council Starting Grants (ERC-2010-StG). Project Endofood "Neurocircuitry of endocannabinoid control of food intake"

2007: Award for Young Investigators International Association for Cannabis as Medicine

2006: AVENIR Price of Fondation Bettencourt- Schueller

2002: Price for Best Presentation of the Meeting at the 12th Symposium on the Cannabinoids.

Monterey, Pacific Grove, California (USA), Jul. 10-14, 2002.

Recent main fundings

AVENIR/Fondation Bettencourt Schueller, 2006-2010

European Research Council (ERC), 2010-2015

EU-FP7 Reprobesity, 2009-2012

Fondation pour la Recherche Medicale (FRM), 2011-2013

Region Aquitaine Council, 2007-2013

ANR, NutriSens, 2013-2016

Scientific summary

The general goal of our group is to understand the cell type-specific role of the endocannabinoid system (ECS) in brain and neuronal functions. The ECS in the brain is formed by the type-1 cannabinoid receptors (CB1), by their endogenous lipid ligands the endocannabinoids (mainly arachidonoyl-ethanolamine, AEA, and 2-arachidonoyl-glycerol, 2-AG), and by the machinery for synthesis and degradation of endocannabinoids.

The major effect of CB1 activation is the decrease of neuronal excitability and the presynaptic reduction of neurotransmitter release. As these receptors are expressed both on GABAergic and glutamatergic terminals, their ability to dampen both inhibitory and excitatory neurotransmission could underlie different and even opposite effects of the ECS on neuronal functions and behaviour. To understand the specific role(s) of CB1 signalling in these two neuronal populations, we developed advanced conditional genetic tools, allowing the deletion of CB1 receptors in specific neuronal populations in mice. Using these tools, we studied the effects of the conditional deletion of CB1 in GABAergic and cortical glutamatergic neurons.

During the last years, we obtained results pointing to the novel idea that the ECS exerts different functions, depending of the cell type-specific expression of CB1. In detail, CB1 receptors on cortical glutamatergic neurons mediate the well-known neuroprotective and orexigenic functions of the ECS and account for some classical effects of CB1 agonists. Surprisingly, the abundant expression of CB1 in GABAergic neurons is not involved in ECS-dependent neuroprotection and in classical effects of CB1 agonists, but it mediates so-far unsuspected pro-neophobic and anorectic functions of the ECS.

These results provided a new vision of the ECS and allowed the publication of interesting articles. They also constitute the ground for our future projects, in which the polymodal mechanisms of action of the ECS will be further detailed and investigated.

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