Date event : December 8, 2017 - 11:00am Conference / Talk Published on 11/24/2017 - 1:59pm
Over the years, balance of excitation and inhibition (E/I) have provided a simplistic view of synaptic computation and its alteration in neurological disorders. Recent advances in understanding neural circuits that processes sensory information have revealed that even during normal physiological function, magnitude and direction of changes in excitation and inhibition is extremely dynamic to support ongoing neural computation. In this talk, I will present evidences from Rett syndrome (RTT), a neurological disorder arising from loss of function mutations in _Mecp2_, how the functional effects of MeCP2 in inhibitory interneuron subtypes critically control visual information processing by non-cell autonomously affecting target cell response specificity and selectivity. _Mecp2 _deletion also alters cellular Cl- balance further impacting effectiveness of early inhibition. Administration of human recombinant IGF-1 (rhIGF1), a drug in Phase-II clinical trial, cell-type specifically restores cellular and circuit defects. Thus, loss of MeCP2 from specific interneuron types contributes crucially to the cell-specific and circuit-wide deficits in RTT, suggesting that targeting such neurons will offer a mechanism-based therapeutic role for rhIGF1 in treating RTT. Finally, I will discuss new approaches using awake behaving animals to study behavioural flexibility defects in learning dynamics in neurological disorders.
Marie Curie Fellow
NARSAD Young Investigator
Laboratory of Neural Circuit Dynamics
Brain Research Institute
University of Zürich
Invited by Equipe Dehay