Our research interests have focused on the molecular mechanism of the regulated secretory process and the pathogenesis of Parkinson’s disease (PD). Our laboratory has been using chromaffin cells and PC12 cells as model systems to study the molecular machinery of Ca²⁺-dependent exocytosis for many years. The accumulated information and experience in the study of these catecholaminergic cells have prompted our study moving from the mechanistic study in model systems to the understanding of the dopamine system in brain under physiological and pathological conditions, mainly PD in which the degeneration of dopaminergic neurons is the primary cause. Our research focuses on the role of α-synuclein in the pathogenesis of PD. The specific projects currently working in the laboratory are:

• Role of α-synuclein in regulated secretion - We have performed a detailed characterization of the role of Rab3A and its relationship with Munc13 and Munc18 during vesicle priming before the occurrence of exocytosis based on the total internal reflection fluorescence microscope images obtained. α-Synuclein is a protein that present in Lewy body and Lewy neurites. Evidence supports that α-synuclein is involved in neurotransmitter release by regulated secretion. The goal is to clearly define how α-synuclein interacts with the individual molecules and where α-synuclein acts in the various steps occurred during exocytosis.
• Association between the physiological function of α-synuclein and the degeneration of DA neurons - We have characterized the Ca²⁺ signaling pathways in primary cultured mouse mesencephalic dopaminergic neurons and established two animal models for the study of pathogenesis of PD: an “aging” version of the well accepted MPP⁺-induced dopaminergic neuron degeneration mouse model and a Zn²⁺ and dopamine-induced striatal dopamine depletion mouse model based on our previous results. We are using the two mouse models to study the association between the physiological function of α-synuclein and the pathogenesis of PD.