What is it about?

Our study strengthens the conclusion that midbrain dopamine neurons release the neurotransmitter GABA and indicate that the vast majority of dopamine neurons participate in GABA co-release. Importantly, we show that SNc and VTA neurons do not synthetize GABA de novo, but instead acquire it from the extracellular milieu using membrane transporters.

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Why is it important?

Our findings not only challenge the notion that all GABAergic neurons express GABA synthetic enzymes, it also suggests that dopamine neurons may be able to control GABAergic transmission locally across their extensive axonal arbors. In addition, our study paves the way for the development of tools to dissect the specific contribution of GABA co-release to striatal function.

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This page is a summary of: Midbrain dopamine neurons sustain inhibitory transmission using plasma membrane uptake of GABA, not synthesis, eLife, April 2014, eLife,
DOI: 10.7554/elife.01936.
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