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

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Wang, L; Nadler, JV

Published Date

  • February 2, 2007

Published In

Volume / Issue

  • 412 / 3

Start / End Page

  • 239 - 242

PubMed ID

  • 17123709

International Standard Serial Number (ISSN)

  • 0304-3940

Digital Object Identifier (DOI)

  • 10.1016/j.neulet.2006.11.006

Language

  • eng

Conference Location

  • Ireland