Aspartate release and signalling in the hippocampus.

Journal Article (Journal Article;Review)

The Ca(2+)-dependent release of aspartate from hippocampal preparations was first reported 35 years ago, but the functional significance of this process remains uncertain. Aspartate satisfies all the criteria normally required for identification of a CNS transmitter. It is synthesized in nerve terminals, is accumulated and stored in synaptic vesicles, is released by exocytosis upon nerve terminal depolarization, and activates postsynaptic NMDA receptors. Aspartate may be employed as a neuropeptide-like co-transmitter by pathways that release either glutamate or GABA as their principal transmitter. Aspartate mechanisms include vesicular transport by sialin, vesicular content sensitive to glucose concentration, release mainly outside the presynaptic active zones, and selective activation of extrasynaptic NR1-NR2B NMDA receptors. Possible neurobiological functions of aspartate in immature neurons include activation of cAMP-dependent gene transcription and in mature neurons inhibition of CREB function, reduced BDNF expression, and induction of excitotoxic neuronal death. Recent findings suggest new experimental approaches toward resolving the functional significance of aspartate release.

Full Text

Duke Authors

Cited Authors

  • Nadler, JV

Published Date

  • April 2011

Published In

Volume / Issue

  • 36 / 4

Start / End Page

  • 668 - 676

PubMed ID

  • 20953700

Electronic International Standard Serial Number (EISSN)

  • 1573-6903

Digital Object Identifier (DOI)

  • 10.1007/s11064-010-0291-3


  • eng

Conference Location

  • United States