Massimo Mantegazza, PhD

The Institute of Molecular and Cellular Phamacology (IPMC) is part of the CNRS Biological Sciences Institute, and is affiliated with CNRS (UMR7275), Inserm (U1323) and Université Côte d’Azur, which is among the most research-oriented universities in France. The IPMC is a multi-thematic institute that performs world class research in the domains of pathophysiology and neuroscience and has state of the art shared facilities on mouse phenotyping, imaging and functional genomics. The IPMC and its affiliations, in particularly the CNRS Côte d’Azur Regional Delegation, have the organizational structure and the ability to transfer technologies to the industry and the socio-economic world.

Beside the PI, the group is formed by three senior researchers (Sandrine Cestèle, CRHC CNRS, Fabrice Duprat, CRCN Inserm, and Fabrizio Capitano, MCU UCA) and a permanent technician (Emilie Bonnet, CNRS), as well as several postdods and PhD students. The group performs interdisciplinary research exploiting molecular biology, biochemistry, electrophysiology, microscopy, behavioral studies and computational modeling. They use in vitro (transfected cells), ex vivo (brain slices) and in vivo (ECoG, LFP, single units) electrophysiological recordings as well as behavioural tests and in vivo chronic treatments to characterize mouse models and identify pathological mechanisms and therapies, using state of the art facilities for electrophysiological recordings and mouse phenotyping.

Expert of experimental models of developmental and epileptic encephalopathies.

Dr. Mantegazza is Inserm Research Director and Team Leader at the IPMC. He is an internationally-recognized expert in the study of ion channels, of the pathophysiology of neuronal excitability, and of the mechanism of action of antiepileptic drugs. His group has developed and characterized experimental models of pathogenic mutations causing neurodevelopmental diseases, including models of developmental and epileptic encephalopathies, identifying specific defects in neuronal functions and their consequences on network excitability and phenotype.

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Main publications:

• Preictal dysfunctions of inhibitory interneurons paradoxically lead to their rebound hyperactivity and to low-voltage-fast onset seizures in Dravet syndrome, PNAS, 2024.
• The gain of function SCN1A disorder spectrum: novel epilepsy phenotypes and therapeutic implications, Brain 2022.
• Initiation of migraine-related cortical spreading depolarization by hyperactivity of GABAergic neurons and NaV1.1 channels, Journal of clinical investigation, 2021.
• Sodium channelopathies of skeletal muscle and brain, Physiological review, 2021.
• Na_V1.2 haploinsufficiency in Scn2a knock-out mice causes an autistic-like phenotype attenuated with age, Scientific reports, 2019.
• A two-hit story: Seizures and genetic mutation interaction sets phenotype severity in SCN1A epilepsies, Neurobiology of disease, 2019.
• Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy, Nature Neuroscience, 2006.