SeminarPast EventNeuroscience

SCN1A/Nav1.1 sodium channel: loss and gain of function in epilepsy and migraine

Schedule
Wednesday, April 21, 2021
16:00 UTC
Massimo Mantegazza

Prof

Institute of Molecular and Cellular Pharmacology (IPMC) CNRS UMR7275 and University Côte d'Azur

Host: Clinical and Experimental Epilepsy

Event Information

Host

Clinical and Experimental Epilepsy

Duration

70 minutes

Abstract

Genetic mutations of the SCN1A gene, the voltage gated sodium channel NaV1.1, cause well-defined epilepsies, including the severe developmental and epileptic encephalopathy Dravet syndrome and genetic epilepsy with febrile seizures plus (GEFS+), as well as a severe form of migraine with aura, familial hemiplegic migraine (FHM). More recently, they have been identified in an extremely severe early infantile encephalopathy. Functional studies and animal models have contributed to disclose pathological mechanisms, which can be often linked to a straightforward loss- vs gain- of channel function. However, although this simple dichotomy is pertinent and useful, detailed pathological mechanisms in neuronal circuits can be more complex, sometimes because of unexpected homeostatic or pathologic responses. I will compare pathological mechanisms of epilepsy and migraine mutations studied with cellular, animal and computational models, highlighting a novel homeostatic response implemented by CCK-positive GABAergic neurons in a mouse model of Dravet syndrome, which may be boosted in therapeutic approaches.

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