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Suh, Pann-Ghill
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PLCγ1 in dopamine neurons critically regulates striatal dopamine release via VMAT2 and synapsin III

Kim, Hye YunLee, JieunKim, Hyun-JinJang, Hyun-JunSuh, Pann-GhillKim, Jae-Ick
Issued Date
The 25th Annual Meeting of the Korean Society for Brain and Neural Sciences
Dopamine neurons are essential for voluntary movement, reward learning,
and motivation, whose dysfunction is closely related to various psychological
and 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 did not adversely affect morphology and
structure of midbrain dopamine neurons but did facilitate dopamine release
from dopaminergic axon terminals in the striatum. 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 Brain and Neural Sciences


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