My research investigates the neural circuitry underlying behavior, with a particular focus on the cerebellum and its interactions with cortical and subcortical networks. I examine how circuit-level imbalances give rise to autism-related behavioral deficits, with an emphasis on impairments in social cognition.
Using autism-relevant transgenic mouse models, I pursue a multi-scale experimental strategy that integrates targeted circuit manipulation, in vivo neural activity monitoring, and quantitative behavioral analysis. My work combines optogenetics, chemogenetic, fiber photometry (in vivo calcium imaging), pharmacology, molecular approaches, and behavioral assays, complemented by brain-wide functional connectivity mapping.
I have identified excessive inhibitory drive within cerebellar cortical circuits, leading to reduced Purkinje cell firing, as a key mechanism contributing to autistic-like behaviors. Importantly, enhancing Purkinje neuron activity is sufficient to rescue these behavioral deficits. In parallel, I demonstrate that selective excitation of cerebellar cortical interneurons disrupts social recognition memory, particularly during the retrieval phase, and is accompanied by disorganization of large-scale brain networks.
Together, these findings establish the cerebellum as an active regulator of social cognition rather than a purely motor structure, and identify cerebellar circuit tuning as a mechanistically grounded entry point for therapeutic intervention in psychiatric disorders.