研究人員｜中央研究院 細胞與個體生物學研究所

Our research focuses on the stability and plasticity of neural circuits and the altered sensory circuits in neuropsychiatric disorders

1.  Stability and flexibility of sensory circuits

Neural activity continuously evolves even without new learning or perturbation. This representational drift is present across different cortical areas, and it may reflect the dynamic equilibrium of learning and memory and benefit neural computation. We study the mechanisms and functions of drift in the mouse's primary somatosensory cortex (S1) using chronic Ca2+ imaging on awake, behaving animals. We will explore the links between representational drift, behavioral requirements, plasticity, and neural connectivity.

2.  Cell types-specific involvement in neural plasticity

The advent of single-cell transcriptomics has classified neurons into distinct cell types based on their genetic profiles. However, the link between the cell types and their anatomical or functional properties is largely unknown. We will combine Ca2+ imaging, viral tracing, and spatial transcriptomics to investigate the specific role of each genetically defined cell type during sensory processing, learning, and development.

 3.   Altered sensory coding in autism spectrum disorder

Atypical sensory processing occurs in up to 90% of individuals with autism spectrum disorder (ASD), so sensory cortices are valuable places to study circuit dysfunction in autism. Although a dominant circuit-level model has suggested hyperexcitability and excessive pyramidal spikes in ASD, increased spiking is uncommon in sensory cortices. Instead, various forms of degraded neural coding have been observed. Our current goal is to characterize neural coding phenotypes in the S1 of ASD mouse models with different degrees of hyperexcitability at the synaptic level. This work could verify the consensus and divergence between autism subtypes.