Research Group Lab Hall
Sang Lee, PhD

Sang H. Lee, PhD



  • Pharmacology and Toxicology

Contact Information

General Interests



PhD, Biochemistry, Gyeongsang National University, South Korea, 1998

Research Interests

Synapses are fundamental functional units of neurons. Dynamic remodeling of synapses by the addition of new synapses or the elimination of existing synapses is crucial for neural circuit function and information storage. Aberrant synapse loss is directly associated with multiple neuropsychological diseases including major depressive disorder and Alzheimer’s disease. However, molecular mechanisms involved in synapse loss are yet poorly understood. The long-term goal of my research program is to understand molecular and cellular mechanisms of synaptic plasticity, especially the ones relevant to synapse weakening and loss. Our current research projects focus on recently identified two novel secreted factors that have profound effect on excitatory and GABAergic synapses, respectively. We use a multidisciplinary approach that include biochemistry, molecular biology, cell biology, a variety of imaging techniques (confocal, two-photon, super-resolution, and real time-imaging), electrophysiology, behavioral tests, and mouse genetics.

Activity-dependent Remodeling of Excitatory Synapses

We recently identified a neuronal protein, Proline-rich 7 (PRR7), as a novel Wnt inhibitor that promotes excitatory synapse loss in local neurons. Remarkably, PRR7 is secreted via extracellular vesicles called exosomes in an activity-dependent manner. Exosomes containing elevated levels of PRR7 are absorbed by neurons and promotes the loss of excitatory synapses in recipient neurons. We are investigating the molecular mechanisms by which PRR7 induces the loss of excitatory synapses. In addition, we study the potential role of PRR7 in the synapse loss associated with neurodegenerative diseases including Alzheimer’s disease.

Activity-dependent Modulation of Inhibitory Synapses

Inhibitory synaptic transmission via GABAergic synapses is critical for shaping network activity and maintaining neural circuit functionality. Defective and aberrant GABAergic synapses are associated with multiple neuropsychological conditions including mood disorders. However, molecular mechanisms involved in the regulated elimination of inhibitory synapses are poorly understood. TAFA2 is a brain-specific, novel chemokine-like protein expressed by neurons. Our recent studies using TAFA2 gene knockout animals indicate that TAFA2 is involved in anxiety and fear responses. We are investigating the mechanism and signaling pathways by which TAFA2 induces the loss of GABAergic synapses.