Release-regulating D-2 dopamine receptors are located on striatal glutamatergic nerve terminals.

The effects of dopamine (DA) and other dopaminergic receptor agonists on the depolarization-evoked release of endogenous glutamic acid (GLU) have been studied using synaptosomes prepared from rat corpus striatum and depolarized in superfusion with 15 mM KCl. DA and the selective D-2 receptor agonists quinpirole (LY-171555, the levorotatory enantiomer of LY-141865) and pergolide inhibited GLU release in a concentration-dependent way. The natural agonist was particularly effective causing 50% inhibition of GLU release at 10 nM. In contrast, the selective D-1 receptor agonist SK&F 38393 did not affect the release of GLU. The inhibitory effect of DA on the K+-evoked release of GLU was antagonized in a concentration-dependent manner by the selective D-2 receptor antagonist S-sulpiride, but not by the R-enantiomer. The data represent a direct demonstration that receptors sensitive to nanomolar concentrations of DA and belonging to the D-2 type are located on GLU axon terminals in the rat corpus striatum where they may modulate the release of GLU from glutamatergic afferents including the cortico-striatal pathway.

• Publication year

  1988

• Venue

  Journal of Pharmacology and Experimental Therapeutics

• Publication date

  1988-11-01

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.1016/s0022-3565(25)13418-6PMID 2903237
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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