Neuronal Depolarization Drives Increased Dopamine Synaptic Vesicle Loading via VGLUT.

ABSTRACT: The ability of presynaptic dopamine terminals to tune neurotransmitter release to meet the demands of neuronal activity is critical to neurotransmission. Although vesicle content has been assumed to be static, in vitro data increasingly suggest that cell activity modulates vesicle content. Here, we use a coordinated genetic, pharmacological, and imaging approach in Drosophila to study the presynaptic machinery responsible for these vesicular processes in vivo. We show that cell depolarization increases synaptic vesicle dopamine content prior to release via vesicular hyperacidification. This depolarization-induced hyperacidification is mediated by the vesicular glutamate transporter (VGLUT). Remarkably, both depolarization-induced dopamine vesicle hyperacidification and its dependence on VG

SUBMITTER: Aguilar JI 

PROVIDER: S-EPMC5760215 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature