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DEVELOPMENTAL DYNAMICS OF CORTICAL NETWORKS IN FOCAL CORTICAL DYSPLASIA TYPE II: INSIGHTS FROM IN VIVO TWO-PHOTON CALCIUM IMAGING
Léo Goldsteinand 4 co-authors
INMED U249
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-380
Presentation
Date TBA
Board: PS05-09AM-380
Event Information
Poster Board
PS05-09AM-380
Poster
View posterAbstract
Focal cortical dysplasia type II (FCD II) is a frequent cause of pharmacoresistant epilepsy driven by hyperactivation of the mTOR signaling pathway and abnormal cortical development. While the structural and cellular features of FCD II are well characterized, the circuit level mechanisms underlying the emergence of pathological network activity remain poorly understood.
This project investigates the maturation of neuronal networks in the somatosensory cortex using a mouse model of FCD II generated by in utero electroporation of a consitutively active mTOR mutant. To characterize network maturation, we performed longitudinal in vivo two-photon calcium imaging in awake mice, synchronized with behavioral videography. This approach allowed us to assess both spontaneous network dynamics and activity evoked by controlled whisker stimulation throughout development and adulthood.
By adopting a developmental network-level approach, this study seeks to identify the critical periods and underlying mechanisms that drive the onset of pathological activity in FCD II. Notably, it provides a framework for dissecting how alterations in glutamatergic signaling lead to network dysfunction and epileptiform activity in the dysplastic cortex.
This project investigates the maturation of neuronal networks in the somatosensory cortex using a mouse model of FCD II generated by in utero electroporation of a consitutively active mTOR mutant. To characterize network maturation, we performed longitudinal in vivo two-photon calcium imaging in awake mice, synchronized with behavioral videography. This approach allowed us to assess both spontaneous network dynamics and activity evoked by controlled whisker stimulation throughout development and adulthood.
By adopting a developmental network-level approach, this study seeks to identify the critical periods and underlying mechanisms that drive the onset of pathological activity in FCD II. Notably, it provides a framework for dissecting how alterations in glutamatergic signaling lead to network dysfunction and epileptiform activity in the dysplastic cortex.
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