We are interested in understanding how sensory experience can be accurately translated into neuronal and behavioral plasticity through genetic and epigenetic networks. Sensory experience-evoked neural activity plays essential roles in brain development and function, not only by instructing structural and functional changes in individual synapses but also by triggering various calcium-dependent signaling cascades which ultimately lead to the activation of specific gene expression programs in the nucleus. This activity-induced nuclear gene expression is the cell-wide adaptation mechanism that permits the synaptic and behavioral plasticity to be long-lasting. Many key players in the programs have been implicated in several human neurological disorders such as Autism Spectrum Disorder (ASD) and epilepsy. It is our hope to provide novel mechanistic insights into the etiology of these relevant disorders.