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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Resources
Midbrain neurons recycle GABA
Many dopamine neurons in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) signal to striatal projection neurons (SPNs). Mounting evidence indicates that these dopaminergic neurons co-release other neurotransmitters, although the details of this co-transmission remain to be fully established. In a new study, Sabatini and colleagues show that dopaminergic midbrain neurons co-release GABA and that, surprisingly, the source of this neurotransmitter is extracellular.
eLife DIgest
Previous research showed that some of the midbrain neurons activate receptors that normally respond to a neurotransmitter called gamma-aminobutyric acid (GABA). However, several different chemicals can trigger this receptor. Using a range of techniques, Tritsch et al. now confirm that dopamine neurons release GABA alongside dopamine, and that this applies to both sets of the dopamine-producing neurons that feed into the striatum.
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