- Anti-oxidant/anti-inflamatory nanoparticles to protect the brain from excess electrophysiology and to mitigate damage post-crisis
- Characterization of the didys552 zebrafish mutant line (mutation in snc1lab gene) and set up of an efficacy drug screening assay using reference compounds
- Cell Therapy with GABAergic interneuron precursors for Early Infantil Epileptic Encephalopathies (S. Dravet, S. West y S. Stxbp1)
- Creation of a therapeutic drug monitoring (TDM) unit for the optimization of the Dravet syndrome pharmacological therapy
- Design, synthesis and pharmacological evaluation of new neuroprotective agents oriented to the tratment of Dravet syndrome
- Efecto de campos magnéticos estáticos de intensidad moderada en modelos de epilepsia y síndrome de Dravet
- The effect of beta-caryophyllene treatment in a murine model of Dravet syndrome
- The endocannabinoid system study in Dravet syndrome
- Intrinsic neuronal excitability and spontaneous 1 activity underlie cortical abnormalities upon Nr2f1/COUP-TFI deficiency
- Investigating Epilepsy by Super-resolution Imaging of Synapses and the Extracellular Space in Live Brain Tissue
- Precision Medicine in Dravet Syndrome
- Reactive Neurogenesis and Gliogenesis in a Dravet Syndrome Mouse Model
(Neural Plasticity Group)
(Neural Plasticity Group)
Intrinsic neuronal excitability and spontaneous 1 activity underlie cortical abnormalities upon Nr2f1/COUP-TFI deficiency.
Scientific Groups: M Studer Lab (Ibv, Nice) and X Leinekugel Lab (INSERM U1215, Bordeaux).
The formation of functionally different areas in the cerebral cortex results from a timely regulated interaction between intrinsic genetic mechanisms and electrical activity. However, whether and how transcriptional regulation influences spontaneous activity intrinsic to the neocortex during critical periods of corticogenesis is poorly elucidated. In the lab, we use mice deficient for cortical Nr2f1 (also known as COUP-TFI) to investigate how a genetic-determinant of somatosensory area-identity linked to epileptic encephalopathy, influences immature neural excitability and network activity generated within the neocortex. Our research unveiled that loss of Nr2f1 alters intrinsic excitability and morphological features of pyramidal neurons during early postnatal stages. We also identified voltage-gated ion channels regulated by Nr2f1 during a critical time window of somatosensory area specification. Accordingly, Nr2f1 loss impacted on spontaneous network activity and synchronization at perinatal stages.
Together, our data suggest that genetic specification of cortical area identity relies on intrinsic bioelectrical properties regulating patterns of spontaneous activity intrinsic to the neocortex early on in cortical development.
Ibv (Nice-Université Côte D´Azur), Neurocentre Magendie INSERM-U1215 (Université de Bordeaux).