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• W3217766078 abstract "Dopamine (DA)-releasing neurons in the substantia nigra pars compacta (SNcDA) inhibit target cells in the striatum through postsynaptic activation of γ-aminobutyric acid (GABA) receptors. However, the molecular mechanisms responsible for GABAergic signaling remain unclear, as SNcDA neurons lack enzymes typically required to produce GABA or package it into synaptic vesicles. Here we show that aldehyde dehydrogenase 1a1 (Aldh1a1), an enzyme proposed to function as a GABA synthetic enzyme in SNcDA neurons does not produce GABA for synaptic transmission. Instead, we demonstrate that SNcDA axons obtain GABA exclusively through presynaptic uptake using the membrane GABA transporter Gat1 (encoded by Slc6a1). GABA is then packaged for vesicular release using the vesicular monoamine transporter Vmat2. Our data therefore show that presynaptic transmitter recycling can substitute for de novo GABA synthesis and that Vmat2 contributes to vesicular GABA transport, expanding the range of molecular mechanisms available to neurons to support inhibitory synaptic communication." @default.
• W3217766078 created "2021-12-06" @default.
• W3217766078 creator A5051644549 @default.
• W3217766078 creator A5065363379 @default.
• W3217766078 date "2021-11-26" @default.
• W3217766078 modified "2023-10-16" @default.
• W3217766078 title "Inhibitory co-transmission from midbrain dopamine neurons relies on presynaptic GABA uptake" @default.
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• W3217766078 doi "https://doi.org/10.1101/2021.11.26.470142" @default.
• W3217766078 hasPublicationYear "2021" @default.
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