Presynaptic glutamate receptors modulate dopamine release from striatal synaptosomes

J Neurochem. 1991 Sep;57(3):819-22. doi: 10.1111/j.1471-4159.1991.tb08224.x.

Abstract

The wide-ranging neuronal actions of glutamate are thought to be mediated by postsynaptic N-methyl-D-aspartate (NMDA) and non-NMDA receptors. The present report demonstrates the existence of presynaptic glutamate receptors in isolated striatal dopaminergic nerve terminals (synaptosomes). Activation of these receptors, by NMDA in the absence of Mg2+ and presence of glycine and by non-NMDA agonists in the presence of Mg2+, results in Ca(2+)-dependent release of dopamine from striatal synaptosomes. The release stimulated by NMDA is blocked by Mg2+ and by selective NMDA antagonists, whereas the release stimulated by selective non-NMDA agonists is blocked by a non-NMDA antagonist but not by Mg2+ or NMDA antagonists. Thus, these presynaptic glutamate receptors, localized on dopaminergic terminals in the striatum, appear to be pharmacologically similar to both the NMDA and the non-NMDA postsynaptic receptors. By modulating the release of dopamine, these presynaptic receptors may play an important role in transmitter interactions in the striatum.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / pharmacology
  • Corpus Striatum / ultrastructure*
  • Dopamine / metabolism*
  • Glycine / pharmacology
  • Magnesium / pharmacology
  • Male
  • Rats
  • Rats, Inbred Strains
  • Receptors, Glutamate
  • Receptors, Neurotransmitter / physiology*
  • Synaptosomes / metabolism*
  • Synaptosomes / ultrastructure
  • Tritium

Substances

  • Receptors, Glutamate
  • Receptors, Neurotransmitter
  • Tritium
  • Magnesium
  • Calcium
  • Glycine
  • Dopamine