RT Journal Article SR Electronic T1 Opponent vesicular transporters regulate the strength of glutamatergic neurotransmission in a C. elegans sensory circuit JF bioRxiv FD Cold Spring Harbor Laboratory SP 2021.03.20.436253 DO 10.1101/2021.03.20.436253 A1 Jung-Hwan Choi A1 Lauren Bayer Horowitz A1 Niels Ringstad YR 2021 UL http://biorxiv.org/content/early/2021/03/22/2021.03.20.436253.abstract AB At chemical synapses, neurotransmitters are packaged into synaptic vesicles that release their contents in response to depolarization. Despite its central role in synaptic function, regulation of the machinery that loads vesicles with neurotransmitters remains poorly understood. We find that synaptic glutamate signaling in a C. elegans chemosensory circuit is regulated by antagonistic interactions between the canonical vesicular glutamate transporter EAT-4/VGLUT and another vesicular transporter, VST-1. Loss of VST-1 strongly potentiates glutamate release from chemosensory BAG neurons and disrupts chemotaxis behavior. Analysis of the circuitry downstream of BAG neurons shows that excess glutamate release disrupts behavior by inappropriately recruiting RIA interneurons to the BAG-associated chemotaxis circuit. Our data indicate that in vivo the strength of glutamatergic synapses is controlled by regulation of neurotransmitter packaging into synaptic vesicles via functional coupling of VGLUT and VST-1.Competing Interest StatementThe authors have declared no competing interest.