Plasticity

The complexity of the neuronal connections is formed during development under the guidance of both genetic and environmental factors. The interplay between genetic blueprint and neuronal activity results in formation of synaptic connections pattern, unique for each individual. Genetic or environmental alterations in this process may push developing network towards pathological attractor state, leading to progression of a neurodevelopmental disorder.

My research has investigated neurobiology of neurodevelopmental disorders, especially autism spectrum disorder, using fragile X syndrome (FXS) as a model disease. We have shown that the absence of FMR1 protein affects differentiation of human and mouse FXS neural progenitors leading changes in calcium dynamics and functional responses of differentiated neuronal cells.

My lab investigates neurobiological mechanisms underlying rapid antidepressant effects. We have recently revealed that diverse rapid-acting antidepressants evoke – after the acute pharmacological effects subside – an emergence of slow EEG activity (SWA) and concomitant regulation of plasticity-related molecular pathways (e.g. TrkB neurotrophin receptor) in adult rodents. These findings urge to focus on intrinsic homeostatic adaptations triggered within the brain in response to pharmacological or physiological “challenge” induced by rapid-acting antidepressants.