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Role of nitric-oxide in nmda-evoked release of h-3 dopamine from striatal slices

Academic Article
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Overview

authors

  • Hanbauer, I.
  • Wink, D.
  • Osawa, Y.
  • Edelman, Gerald
  • Gally, J. A.

publication date

  • May 1992

journal

  • Neuroreport  Journal

abstract

  • Evidence that excitatory amino acids act via N-methyl-D-aspartate (NMDA) receptors to evoke the release of catecholamines from axonal terminals and synaptosomes has been used to argue for the presence of pre-synaptic NMDA receptors. NMDA receptor agonists also generate nitric oxide (NO) which rapidly diffuses through neural tissue. We find that exogenously applied NO evokes [3H]-dopamine release from cultured neurons. This release is not blocked by the NMDA antagonist MK-801 nor by tetrodotoxin. Both NG-nitroarginine which inhibits NO synthesis, and hemoglobin which binds extracellular NO, block NMDA-evoked [3H]-dopamine release from striatal slices. A major role of endogenously-synthesized NO may be to evoke neurotransmitter release in local volumes of neural tissue.

subject areas

  • Animals
  • Cells, Cultured
  • Corpus Striatum
  • Dopamine
  • Female
  • In Vitro Techniques
  • N-Methylaspartate
  • Nitric Oxide
  • Rats
  • Rats, Inbred Strains
  • Tritium
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Research

keywords

  • CATECHOLAMINE
  • NEUROTRANSMITTER RELEASE
  • PRESYNAPTIC RECEPTORS
  • SPATIAL SIGNAL
  • STRIATUM
  • TETRAHYDROBIOPTERIN
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Identity

International Standard Serial Number (ISSN)

  • 0959-4965

Digital Object Identifier (DOI)

  • 10.1097/00001756-199205000-00008

PubMed ID

  • 1633278
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Additional Document Info

start page

  • 409

end page

  • 412

volume

  • 3

issue

  • 5

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