Research in my laboratory focuses on dissecting the mechanisms underlying Brain Development. Using rodent models, we study the influence of genetic and environmental factors on dynamic neurodevelopmental processes, such as neurogenesis, cell differentiation & migration, early activity and connectivity. We also assess development in human infants using high-density electroencephalography (hd-EEG) and correlate brain activity with physiological and cognitive tools to help map the developmental time-course and possible deviations in at-risk groups for neurodevelopmental conditions. With this translational approach, we aim to connect basic and clinical components of Developmental Neuroscience and contribute to the early identification and treatment of neurodevelopmental disorders.
A growing body of evidence suggests that the susceptibility to Neurodevelopmental disorders such as Autism Spectrum Disorder (ASD), occur early in embryonic stages and progress throughout postnatal development, when behaviors become evident. To help dissect the possible mechanisms involved in the etiology of ASD, we generate in vivo rodent models by in utero electroporation using vectors to label and/or genetically modify gene expression in selected cell subsets in the cerebral cortex. Candidate genes are first identified with transcriptomic analyses and compared with pre-existing databases. We then utilize molecular and neuroanatomical tools to carefully map the time-course of gene expression, as well as the cellular and anatomical localization in relation to bonafide markers. Some of the tools employed in the lab include: immunohistochemistry, in situ hybridization and confocal imaging of proliferative and neurogenic niches.
In addition, we are developing in vivo imaging (i.e. calcium imaging through miniscopes) and electrophysiological tools (LFP, scalp EEG recordings) to assess the impact of genetic and environmental insults during postnatal development in rodents. We are particularly interested in exploring the hypothesized link between anatomical malformations (e.g. dysplasia, tubers or calcifications, usually caused by genetic/environmental insults) and the emergence of aberrant activity during brain development. The identification of anatomical correlates of typical and atypical brain activity patterns in rodent models may reveal key functions not evident beyond the time-window of brain development, and provide hints to similarities in human conditions.