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Updated: Oct 8, 2026

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs
Published on: August 31, 2009
Release of D,L-threo-beta-hydroxyaspartate as a false transmitter from excitatory amino acid-releasing nerve
M W Fleck1, G Barrionuevo, A M Palmer
1Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Abstract:
This study examined whether preaccumulated D,L-threo-beta-hydroxyaspartate (tHA), a competitive substrate for the high-affinity excitatory amino acid (EAA) transporter, is released as a false transmitter from EAA-releasing nerve terminals. Potassium-stimulation (50 mM for 1 min) evoked significant release of the endogenous EAAs (aspartate and glutamate) from superfused neocortical minislices. Endogenous EAA release was largely calcium-dependent and was inhibited by tetanus toxin, a neurotoxin which specifically blocks vesicular exocytosis. In parallel experiments, minislices were pre-incubated with 500 microM tHA. Potassium (50 mM) evoked significant release of tHA and this release was also calcium-dependent and reduced by tetanus toxin. Pre-accumulation of tHA did not affect the release of endogenous glutamate whereas the release of endogenous aspartate was significantly attenuated. These data suggest that tHA selectively accumulates in a vesicular aspartate pool and is released upon depolarization as a false transmitter from EAA nerve terminals.
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