The Na+-Ca++ exchanger in central nerve endings: The relationship between its pharmacological blockade and dopamine release from tuberoinfundibular hypothalamic neurons

Lucio Annunziato, Maurizio Taglialatela, Lorella M T Canzoniero, Alessandro Fatatis, Gianfranco Di Rienzo

Research output: Contribution to journalArticle

Abstract

2′,4′-Dimethylbenzamiloride (DMB), an inhibitor of Na+-Ca++ antiporter dose-dependently (10-100 μM) inhibited Na+-dependent 45Ca++ efflux from brain synaptosomes. This compound was also able to stimulate basal release of [3H]DA from superfused TIDA neurons. Another amiloride analogue, 5-N-methyl-N-guanidinocarbonylmethylamiloride (MGCMA, 100-300 μM), which lacks of inhibitory properties on the Na+-Ca++ antiporter, failed to modify basal [3H]DA release from TIDA neurons. In addition, when the antiporter operates as a Ca++-influx pathway, DMB dose-dependently inhibited Na+-dependent 45Ca++ uptake in brain synaptosomes, whereas it did not prevent K+-induced 45Ca++ uptake, which reflects the activation of voltage-operated Ca++ channels. Finally DMB inhibited ouabain-induced [3H]DA release, which depends on the activation of the Na+-Ca++ exchanger due to the inhibition of the Na+/K+-ATPase pump.

Original languageEnglish
Pages (from-to)95-99
Number of pages5
JournalNeurochemistry International
Volume20
Issue numberSUPPL.
DOIs
Publication statusPublished - 1992

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

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