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Reduced aspartate release from rat hippocampal synaptosomes loaded with Clostridial toxin light chain by electroporation: evidence for an exocytotic mechanism.

Publication ,  Journal Article
Wang, L; Nadler, JV
Published in: Neurosci Lett
February 2, 2007

Aspartate can be released from certain hippocampal pathways along with glutamate or GABA. Although aspartate immunoreactivity has been localized to synaptic vesicles and aspartate release is Ca(2+)-dependent, there has been no clear evidence favoring an exocytotic mechanism. In particular, pretreatment with Clostridial toxins has not consistently inhibited aspartate release, even when release of glutamate from the same tissue samples was markedly inhibited. To address this issue directly, rat hippocampal synaptosomes were permeabilized transiently by electroporation in the presence of active or inactivated Clostridial toxin light chains. Loading rat hippocampal synaptosomes with the active light chain of tetanus toxin or of botulinum neurotoxins A, B or C reduced the K(+)-evoked release of aspartate at least as much as that of glutamate. These results confirm that aspartate is released by exocytosis in rat hippocampus.

Duke Scholars

Published In

Neurosci Lett

DOI

ISSN

0304-3940

Publication Date

February 2, 2007

Volume

412

Issue

3

Start / End Page

239 / 242

Location

Ireland

Related Subject Headings

  • Tetanus Toxin
  • Synaptosomes
  • Rats
  • Potassium Chloride
  • Neurotoxins
  • Hippocampus
  • Glutamic Acid
  • Female
  • Electroporation
  • Dose-Response Relationship, Drug
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Journal cover image

Published In

Neurosci Lett

DOI

ISSN

0304-3940

Publication Date

February 2, 2007

Volume

412

Issue

3

Start / End Page

239 / 242

Location

Ireland

Related Subject Headings

  • Tetanus Toxin
  • Synaptosomes
  • Rats
  • Potassium Chloride
  • Neurotoxins
  • Hippocampus
  • Glutamic Acid
  • Female
  • Electroporation
  • Dose-Response Relationship, Drug