Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 39, Issue 1, Pages 75-81Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0197-0186(00)00111-X
Keywords
D,L-threo-beta-hydroxyaspartate; excitatory amino acid; synaptic transmission
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Funding
- NIA NIH HHS [AG08974-01] Funding Source: Medline
- NIMH NIH HHS [MH45156] Funding Source: Medline
- NINDS NIH HHS [NS24288] Funding Source: Medline
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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 muM 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. (C) 2001 Elsevier Science Ltd. All rights reserved.
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