First-pass extracted concept

GABA co-release by midbrain dopaminergic neurons

Candidate: concept label1 source documents4 linked claims
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Evidence Snippets

These findings therefore indicate that GABA co-release is a general feature of midbrain dopaminergic neurons that relies on GABA uptake from the extracellular milieu as opposed to de novo synthesis.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1functional implicationsupports2014Source 1DOIPubMed

The uptake-based mechanism may allow dopaminergic neurons to differentially control GABAergic transmission in a target-dependent manner across their axonal arbors.

Quoted textsource-backed
This atypical mechanism may confer dopaminergic neurons the flexibility to differentially control GABAergic transmission in a target-dependent manner across their extensive axonal arbors.
Claim 2mechanismsupports2014Source 1DOIPubMed

GABA co-release by midbrain dopaminergic neurons relies on extracellular GABA uptake rather than de novo synthesis.

Quoted textsource-backed
These findings therefore indicate that GABA co-release is a general feature of midbrain dopaminergic neurons that relies on GABA uptake from the extracellular milieu as opposed to de novo synthesis.
Claim 3mechanismsupports2014Source 1DOIPubMed

Mesolimbic afferents from midbrain dopamine neurons also release GABA.

Quoted textsource-backed
Here, we demonstrate that this phenomenon extends to mesolimbic afferents, and confirm that the released neurotransmitter is GABA.
Claim 4perturbation effectsupports2014Source 1DOIPubMed

Inhibition of mGAT1 and mGAT4 prevents GABA co-release from midbrain dopamine neurons.

Quoted textsource-backed
inhibition of these transporters prevents GABA co-release