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Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
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PLCγ1 in dopamine neurons critically regulates striatal dopamine release via VMAT2 and synapsin III

Lee, JieunKim, Hye YunKim, Hyun-JinJang, Hyun-JunSuh, Pann-GhillKim, Jae-Ick
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Dopamine neurons are essential for voluntary movement, reward learning, and motivation, whose dysfunction is
closely related to various neurodegenerative diseases. Therefore, understanding the detailed signaling mechanisms
functionally modulating dopamine neurons is crucial for the development of better therapeutic strategies against
dopamine-related disorders. In this study, we investigate the physiological role of phospholipase Cγ1 (PLCγ1), one
of the key effector enzymes in intracellular signaling, on regulating dopaminergic function in vivo. We found that cell
type-specific deletion of PLCγ1 facilitated dopamine release from dopaminergic axon terminals. Elevated dopamine
release was accompanied by increased co-localization of vesicular monoamine transporter 2 (VMAT2) at
dopaminergic axons. Notably, dopamine neuron-specific knockout of PLCγ1 also led to the heightened expression
and co-localization of synapsin III that controls the trafficking of synaptic vesicles. Our findings suggest that PLCγ1 in
dopamine neurons could critically modulate dopamine release at axon terminals by directly or indirectly interacting
with synaptic machinery including VMAT2 and synapsin III.
Korean Society for Molecular and Cellular Biology


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