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Research Interests

• During the peak of synaptogenesis, general anesthetics that either block excitatory NMDA glutamate receptors or potentiate inhibitory GABAA receptors can trigger widespread apoptotic neurodegeneration and demyelinating injuries. The mechanisms of this vulnerable window of general anesthesia-induced neurotoxicity remain largely elusive. In our group, we use patch-clamp recording, calcium imaging, molecular biology techniques, etc. to explore the mechanisms of general anesthesia-induced neurotoxicity during the early development, mainly focuses on: 1) the effects of extracellular matrix environment on neuronal apoptosis and demyelination induced by general anesthesia; 2) the interaction between neuronal activity and oligodendrocyte precursor cell during general anesthesia-induced neurotoxicity.