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

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 and Gianfranco Di Rienzo
Neurochemistry international, v 20(MAR), pp 95-99
1992
PMID: 1365465

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.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Neurosciences
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